Luming Liu

Fudan University, Shanghai, Shanghai Shi, China

Are you Luming Liu?

Claim your profile

Publications (29)90.23 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic cancer is unresectable in over 80 % of patients owing to difficulty in early diagnosis. Chemotherapy is the most frequently adopted therapy for advanced pancreatic cancer. The development of drug resistance to gemcitabine (GEM), which is always used in standard chemotherapy, often results in therapeutic failure. However, the molecular mechanisms underlying the gemcitabine resistance remain unclear. Therefore, we sought to explore the microRNA-mRNA network that is associated with the development of gemcitabine resistance and to identify molecular targets for overcoming the gemcitabine resistance. By exposing SW1990 pancreatic cancer cells to long-term gemcitabine with increasing concentrations, we established a gemcitabine-resistant cell line (SW1990/GEM) with a high IC50 (the concentration needed for 50 % growth inhibition, 847.23 μM). The mRNA and microRNA expression profiles of SW1990 cells and SW1990/GEM cells were determined using RNA-seq analysis. By comparing the results in control SW1990 cells, 507 upregulated genes and 550 downregulated genes in SW1990/GEM cells were identified as differentially expressed genes correlated with gemcitabine sensitivity. Gene ontology (GO) analysis showed that the differentially expressed genes were related to diverse biological processes. The upregulated genes were mainly associated with drug response and apoptosis, and the downregulated genes were correlated with cell cycle progression and RNA splicing. Concurrently, the differentially expressed microRNAs, which are the important player in drug resistance development, were also examined in SW1990/GEM cells, and 56 differential microRNAs were identified. Additionally, the expression profiles of selected genes and microRNAs were confirmed by using Q-PCR assays. Furthermore, combining the differentially expressed microRNAs and mRNAs as well as the predicted targets for these microRNAs, a core microRNA-mRNA regulatory network was constructed, which included hub microRNAs, such as hsa-miR-643, hsa-miR-4644, hsa-miR-4650-5p, hsa-miR-4455, hsa-miR-1261, and hsa-miR-3676. The predicted targets of these hub microRNAs in the microRNA-mRNA network were also observed in the identified differential genes. As a result, a differential gene and microRNA expression pattern was constructed in gemcitabine-resistant pancreatic cancer cells. Therefore, these data may be useful for the detection and treatment of drug resistance in pancreatic cancer patients, and the microRNA-mRNA network-based analysis is expected to be more effective and provides deep insights into the molecular mechanism of drug resistance.
    Asia-Pacific Journal of Clinical Oncology 02/2015; 10. DOI:10.1007/s13277-015-3097-8 · 1.06 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: To analyses the feasibility and efficacy of high intensity focused ultrasound (HIFU) treatment in patients with inoperable liver cancer. 187 patients were treated with HIFU, of all these patients 116 cases were Primary Liver Cancer (PLC) and 71 cases were Metastatic Liver Cancer (MLC). According to some parameters, such as clinical symptoms, the basis of main organs functional tests, imaging examinations, and progression-free survival (PFS) time to assess the safety and efficacy of HIFU in the treatment of liver cancer. 55 patients (29.4%) achieved CR and 73 patients (39.0%) achieved PR, 32 patients (17.1%) had responses of SD, and 27 patients (14.4%) were PD, respectively. Response rates were 90.5% (32 CR + 6 PR/42) in left lobe cancer and 64.1% (22 CR + 62 PR/131) in right lobe cancer. The median PFS for those CR case was 7 months, of PLC was 8 months, of MLC was 5 months. HIFU is effective and feasible in the treatment of liver cancer. It offer a significant noninvasive therapy for local treatment of liver cancer. For those right lobe liver cancers or with poor ultrasonic window, increasing treatment time or repeated treatment may improve the efficiency of HIFU ablation.
    Hepato-gastroenterology 01/2015; 62(137):140-3. · 0.91 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND Greater than 70% of patients with cancer experience chemotherapy-induced nausea and vomiting. In the current study, the authors examined the effects of electrostimulation of the K1 acupoint located on the sole of the foot because it is believed to have the potential to control chemotherapy-induced nausea and vomiting.METHODS In this trial, 103 patients diagnosed with primary or metastatic liver cancer were recruited before transcatheter arterial infusion (TAI) of cisplatin or oxaliplatin and randomized to either group A (51 patients who were treated with the antiemetic tropisetron and acustimulation at the K1 acupoint for 20 minutes approximately 1 to 2 hours before TAI on the first day and then daily for the subsequent 5 days) or group B (52 patients who were treated with tropisetron and electrostimulation at a placebo point on the heel). The rate, intensity, and duration of nausea and vomiting were collected at baseline and then daily for 5 days after TAI. Quality of life was assessed daily using the MD Anderson Symptom Inventory and the EuroQoL scale.RESULTSNo differences were found between groups A and B with regard to the incidence and degree of nausea or vomiting on day 1 or the following 5 days. Patients in group A had better EuroQoL scores compared with patients in group B (72.83 in group A vs 65.94 in group B; P =.04) on day 4 but not on the other days. No group differences were noted at any time point for MD Anderson Symptom Inventory scores.CONCLUSIONS Electrostimulation of K1 combined with antiemetics did not result in initial prevention of cisplatin-induced or oxaliplatin-induced nausea or vomiting. Cancer 2014. © 2014 American Cancer Society.
    Cancer 01/2015; 121(1). DOI:10.1002/cncr.28973 · 4.90 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The molecular regulation of the growth of pancreatic carcinoma (PCC) is complicated and not defined yet. Here we show that the cysteine-rich protein 61 (Cyr61) levels were significantly higher in PCC than in the adjacent nontumor tissues from the same human patient. Overexpression of Cyr61 enhanced the proliferation of PCC cells, while inhibition of Cyr61 decreased the proliferation of PCC cells. Further analysis showed that Cyr61 seemed to activate phosphatidylinositol 3-kinase (PI3K) but not extracellular-related kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway in PCC cells, which subsequently induced nuclear exclusion of a major cell cycle inhibitor, p27, to increase cell proliferation. Taken together, these findings reveal the molecular basis underlying Cyr61-regulated PCC proliferation, suggest a potential role of Cyr61 in PCC growth, and highlight Cyr61 as a novel target for PCC therapy.
    Tumor Biology 08/2014; DOI:10.1007/s13277-014-2423-x · 3.61 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: CXCR1, a receptor for CXCL8/IL-8, has recently been demonstrated to be associated with cancer stem cell (CSC) populations in certain types of human cancers. However, the effect of CXCR1 on CSC and its prognostic value in human pancreatic cancer remain unknown. In this study, we evaluated the expression of CXCR1 in human pancreatic duct adenocarcinoma (PDAC) and found that positive CXCR1 expression correlated with lymph node metastasis (P = 0.017) and a poor survival rate (HR, 3.748; 95% CI, 1.822 to 7.712; P < 0.001) in patients with PDAC. In addition, we identified significant positive correlations between CXCR1 and CD44 (P = 0.002) and CD133 (P = 0.017). Further functional studies confirmed that IL-8 addition increased sphere formation, CSC populations, and cell invasion of pancreatic cancer cells and that these effects could be reversed by antagonizing CXCR1 with a CXCR1-specific antibody. Therefore, our study demonstrated that the IL-8/CXCR1 axis is associated with the CSC-like properties of pancratic cancer cells and prognosis in human pancreatic cancer. This suggested a way of targeting pancreatic CSCs by disrupting IL-8/CXCR1 axis.
    Scientific Reports 08/2014; 4:5911. DOI:10.1038/srep05911 · 5.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic cancer remains one of the leading causes of cancer-related deaths, due to aggressive growth, high metastatic rates during the early stage and the lack of an effective therapeutic approach. We previously showed that Qingyihuaji (QYHJ), a seven-herb Chinese medicine formula, exhibited significant anti-cancer effects in pancreatic cancer, associated with modifications in the tumor microenvironment, particularly the inhibition of cancer-associated fibroblast (CAF) activation. In the present study, we generated CAF and paired normal fibroblast (NF) cultures from resected human pancreatic cancer tissues. We observed that CAFs exhibited an enhanced capacity for inducing pancreatic cancer cell migration and invasion compared with NFs, while QYHJ-treated CAFs exhibited decreased migration and invasion-promoting capacities in vitro. The results of further analyses indicated that compared with NFs, CAFs exhibit increased CXCL1, 2 and 8 expression, contributing to the enhanced invasion-promoting capacities of these cells, while QYHJ treatment significantly suppressed CAF proliferation activities and the production of CAF-derived CXCL1, 2 and 8. These in vitro observations were confirmed in mice models of human pancreatic cancer. Taken together, these results suggested that suppressing the tumor-promoting capacity of CAFs through Chinese herbal medicine attenuates pancreatic cancer cell invasion.
    PLoS ONE 04/2014; 9(4):e96177. DOI:10.1371/journal.pone.0096177 · 3.53 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Early metastasis is a major biological feature of pancreatic cancer. The current study examined whether silencing Slc38a1, a gene involved in energy metabolism, using short hairpin RNA (shRNA) could inhibit the growth, migration, and invasiveness of pancreatic cancer cells. A series of Slc38a1 shRNAs were designed and cloned into the pGPU6/GFP/Neo vectors. An shRNA with the most efficacious inhibitory action on SCL38A1 expression (65% inhibition) upon screening in DH5α bacteria was used to transfect SW1990 human pancreatic cancer cells. Cell growth, migration, and invasiveness were examined using cell counting kit-8, Boyden chamber without and with Matrigel, respectively. Transfection of SW1990 cells with the SLCs38A1 shRNA significantly decreased the proliferation (P<0.0001) and migratory potential (by 46.7%, P=0.0399) of the cancer cells. Invasiveness, however, was not affected. Inhibiting Slc38a1 using shRNA technology could decrease the growth and migration of representative pancreatic cancer cells. However, the fact that invasiveness was not affected suggested that SLC38A1 is unlikely to be responsible for early metastasis.
    Chinese Journal of Cancer Research 10/2013; 25(5):514-519. DOI:10.3978/j.issn.1000-9604.2013.09.03 · 0.93 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: It is a therapeutic strategy for cancers including pancreatic to inhibit proteasome activity. Disulfiram (DSF) may bind copper (Cu) to form a DSF-Cu complex. DSF-Cu is capable of inducing apoptosis in cancer cells by inhibiting proteasome activity. DSF is rapidly converted to diethyldithiocarbamate (DDTC) within bodies. Copper(II) absorbed by bodies is reduced to copper(I) when it enters cells. We found that DDTC and copper(I) could form a binuclear complex which might be entitled DDTC-Cu(I), and it had been synthesized by us in the laboratory. This study is to investigate the anticaner potential of this complex on pancreatic cancer and the possible mechanism. Pancreatic cancer cell lines, SW1990, PANC-1 and BXPC-3 were used for in vitro assays. Female athymic nude mice grown SW1990 xenografts were used as animal models. Cell counting kit-8 (cck-8) assay and flow cytometry were used for analyzing apoptosis in cells. A 20S proteasome assay kit was used in proteasome activity analysis. Western blot (WB) and immunohistochemistry (IHC) and terminal deoxynucleotidyl transferase dUTP nick end labeling(TUNEL) assays were used in tumor sample analysis. The results suggest that DDTC-Cu(I) inhibit pancreatic cancer cell proliferation and proteasome activity in vitro and in vivo. Accumulation of ubiquitined proteins, and increased p27 as well as decreased NF-κB expression were detected in tumor tissues of DDTC-Cu(I)-treated group. Our data indicates that DDTC-Cu(I) is an effective proteasome activity inhibitor with the potential to be explored as a drug for pancreatic cancer.
    Toxicology and Applied Pharmacology 09/2013; 273(3). DOI:10.1016/j.taap.2013.09.009 · 3.63 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tumor resistance to radiation is a challenge to treatment of patients with pancreatic cancer. Improving our understanding of the mechanisms of radioresistance could lead to strategies to increase patients' response to therapy. We investigated the roles of microRNAs (miRNAs) involved in radioresistance of pancreatic cancer cells. We established radioresistant pancreatic cancer cell lines and used array analysis to compare levels of different miRNAs between radioresistant cell lines and the parental cell lines from which they were derived. We transfected pancreatic cancer cells with miRNA mimics or inhibitors and evaluated their effects on cell radiosensitivity using a clonogenic survival assay. The effects of miRNA on autophagy were determined by transmission electron microscopy and immunoblot analysis. We used a luciferase reporter assay to identify mRNA targets of specific miRNAs. Radioresistant pancreatic cancer cells had reduced levels of the miRNA MIR23B and increased autophagy, compared with cells that were not radioresistant. Overexpression of MIR23B inhibited radiation-induced autophagy, whereas an inhibitor of MIR23B promoted autophagy in pancreatic cancer cells. Overexpression of MIR23B sensitized pancreatic cancer cells to radiation. The target of MIR23B, ATG12, was overexpressed in radioresistant cells; levels of ATG12 protein correlated with the occurrence of autophagy. Expression of MIR23B blocked radiation-induced autophagy and sensitized pancreatic cancer cells to radiation. We observed an inverse correlation between level of MIR23B and autophagy in human pancreatic cancer tissue samples. In pancreatic cancer cells, reduced levels of the miRNA MIR23B increase levels of ATG12 and autophagy to promote radioresistance. MIR23B might be used to increase the sensitivity of pancreatic cancer cells to radiation therapy.
    Gastroenterology 08/2013; 145(5). DOI:10.1053/j.gastro.2013.07.048 · 13.93 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Pancreatic cancer is an almost universally fatal disease resulting from early invasion of adjacent structures and metastasis and the lack of an effective treatment modality. Our previous studies have shown that Qingyihuaji Formula (QYHJ), a seven-herb Chinese medicine formula, had significant anti-cancer effects in pancreatic cancer. Here, we examined the effects of QYHJ on pancreatic cancer cell invasion and metastasis and the potential associated mechanism(s). We found that QYHJ inhibited both tumor growth and metastasis in nude mice with human pancreatic cancer cell xenografts. Further study indicated that QYHJ inhibited epithelial-to-mesenchymal transition (EMT), which is characterized by increased E-cadherin expression and decreased vimentin, N-cadherin and Slug expression. Interleukin 6 (IL-6), a pro-inflammatory cytokine produced mainly by macrophages, could promote cancer cell EMT and invasion. In contrast, treatment with QYHJ inhibited cancer-related inflammation in tumors by decreasing infiltration of tumor-associated macrophages and IL-6 production, thus preventing cell invasion and metastasis. These results suggested that the Chinese herbal medicine QYHJ could inhibit pancreatic cancer cell invasion and metastasis in part by reversing tumor-supporting inflammation.
    PLoS ONE 07/2013; 8(7):e70334. DOI:10.1371/journal.pone.0070334 · 3.53 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND:Radiotherapy may lead to side effects that undermine patients' quality of life (QOL). Although mind-body practices like qigong appear to improve QOL in cancer survivors, little is known about their benefits for patients who are receiving radiotherapy. Thus, in the current randomized controlled trial, the authors examined the efficacy of a qigong intervention on QOL in women with breast cancer during and after treatment. METHODS:Ninety-six women with breast cancer were recruited from a cancer center in Shanghai, China, and were randomized to a qigong group (N = 49) or a waitlist control group (N = 47). Women in the qigong group attended 5 weekly classes over 5 or 6 weeks of radiotherapy. QOL outcomes (ie, depressive symptoms, fatigue, sleep disturbance, and overall QOL) and cortisol slopes were assessed at baseline, during treatment, at the end of treatment, 1 month later, and 3 months later. RESULTS:The mean age of the women was 46 years (range, 25-64 years). Seven percent of women had stage 0 disease, 25% had stage I disease, 40% had stage II disease, and 28% had stage III disease. Fifty-four percent of women underwent mastectomy. Multilevel analyses revealed that women in the qigong group reported less depressive symptoms over time than women in the control group (P = .05). Women who had elevated depressive symptoms at the start of radiotherapy reported less fatigue (P < .01) and better overall QOL (P < .05) in the qigong group compared with the control group, and these findings were clinically significant. No significant differences were observed for sleep disturbance or cortisol slopes. CONCLUSIONS:The current results indicated that qigong may have therapeutic effects in the management of QOL among women who are receiving radiotherapy for breast cancer. Benefits were particularly evident for patients who had preintervention elevated levels of depressive symptoms. Cancer 2013. © 2013 American Cancer Society.
    Cancer 05/2013; 119(9). DOI:10.1002/cncr.27904 · 4.90 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: miR-21 expression in cancer tissue has been reported to be associated with the clinical outcome and activity of gemcitabine in pancreatic cancer. However, resection is possible in only a minority of patients due to the advanced stages often present at the time of diagnosis, and safely obtaining sufficient quantities of pancreatic tumor tissue for molecular analysis is difficult at the unresectable stages. In this study, we investigated whether the serum level of miR-21 could be used as a predictor of chemosensitivity. We tested the levels of serum miR-21 in a cohort of 177 cases of advanced pancreatic cancer who received gemcitabine-based palliative chemotherapy. We found that a high level of miR-21 in the serum was significantly correlated with a shortened time-to-progression (TTP) and a lower overall survival (OS). The serum miR-21 level was an independent prognostic factor for both the TTP and the OS (HR 1.920; 95% CI, 1.274-2.903, p = 0.002 for TTP and HR 1.705; 95% CI, 1.147-2.535, p = 0.008 for OS). The results from a functional study showed that gemcitabine exposure down-regulated miR-21 expression and up-regulated FasL expression. The increased FasL expression following gemcitabine treatment induced cancer cell apoptosis, whereas the ectopic expression of miR-21 partially protected the cancer cells from gemcitabine-induced apoptosis. Additionally, we confirmed that FasL was a direct target of miR-21. Therefore, the serum level of miR-21 may serve as a predictor of chemosensitivity in advanced pancreatic cancer. Additionally, we identified a new mechanism of chemoresistance mediated by the effects of miR-21 on the FasL/Fas pathway.
    Molecular oncology 11/2012; 7(3). DOI:10.1016/j.molonc.2012.10.011 · 5.94 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background. METHODS: Some studies suggest that acupuncture may be beneficial. Objectives. The authors evaluated the preventive and therapeutic effect of acupuncture for radiation-induced xerostomia among patients with head and neck cancer. Methods. PUBMED, EMBASE, Cochrane Library, CBM, CAJD, Wan Fang database, and VIP Database for Chinese Technical Periodicals were electronically searched, in conjunction with further manual search for relevant articles. Studies that met the inclusion criteria were systematically evaluated. RESULTS: Three randomized controlled trials (RCTs) investigating the therapeutic effect of acupuncture were included. One RCT on the preventive effect of acupuncture was found. Because of the considerable variation among included studies, meta-analysis was not possible. Two included RCTs used placebo controls, and both observed significant improvement in the salivary flow rates between acupuncture and control groups. However, no significant differences were found. Three included RCTs suggested that acupuncture for radiation-induced xerostomia can improve patients' subjective symptoms. The only study evaluating the preventive effect of acupuncture for radiation-induced xerostomia showed positive changes in salivary flow rates (both unstimulated and stimulated) and dry mouth -related symptoms. Acupuncture treatment was well tolerated by all patients and no severe adverse effects were seen. CONCLUSIONS: Insufficient evidence is available to judge whether acupuncture is safe and whether it is effective in preventing or treating radiation-induced xerostomia. Significant research remains to be done before acupuncture can be recommended for routine use in radiation-induced xerostomia.
    Integrative Cancer Therapies 07/2012; 12(3). DOI:10.1177/1534735412451321 · 2.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Xerostomia (dry mouth) after head/neck radiation is a common problem among cancer patients, and available treatments are of little benefit. The objective of this trial was to determine whether acupuncture can prevent xerostomia among head/neck patients undergoing radiotherapy. A randomized, controlled trial among patients with nasopharyngeal carcinoma was conducted comparing acupuncture to standard care. Participants were treated at Fudan University Shanghai Cancer Center, Shanghai, China. Forty patients were randomized to acupuncture treatment and 46 to standard care. Patients were treated 3×/wk on the same days they received radiotherapy. Subjective measures included the Xerostomia Questionnaire and MD Anderson Symptom Inventory-Head and Neck (MDASI-HN). Objective measures were unstimulated and stimulated whole salivary flow rates. Patients were followed for 6 months after the end of radiotherapy. Xerostomia Questionnaire scores for acupuncture were statistically significantly lower than for controls starting in week 3 through the 6 months (P = .003 at week 3, all other P < .0001), with clinically significant differences as follows: week 11, relative risk (RR) 0.63 (95% confidence interval [CI], 0.45-0.87); 6 months, RR 0.38 (95% CI, 0.19-0.76). Similar findings were seen for MDASI-HN scores. Group differences emerged as early as 3 weeks into treatment for saliva (unstimulated whole salivary flow rate, P = .0004), with greater saliva flow in the acupuncture group at week 7 (unstimulated whole salivary flow rate, P < .0001; stimulated whole salivary flow rate, P = .002) and 11 (unstimulated whole salivary flow rate, P < .02; stimulated whole salivary flow rate, P < .03) and at 6 months (stimulated whole salivary flow rate, P < .003). Acupuncture given concurrently with radiotherapy significantly reduced xerostomia and improved quality of life.
    Cancer 07/2012; 118(13):3337-44. DOI:10.1002/cncr.26550 · 4.90 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Xerostomia (dry mouth) after head/neck radiation is a common problem among cancer patients. Quality of life (QOL) is impaired, and available treatments are of little benefit. This trial determined the feasibility of conducting a sham-controlled trial of acupuncture and whether acupuncture could prevent xerostomia among head/neck patients undergoing radiotherapy. A sham controlled, feasibility trial was conducted at Fudan University Shanghai Cancer Center, Shanghai, China among patients with nasopharyngeal carcinoma undergoing radiotherapy. To determine feasibility of a sham procedure, 23 patients were randomised to real acupuncture (N=11) or to sham acupuncture (N=12). Patients were treated three times/week during the course of radiotherapy. Subjective measures were the Xerostomia Questionnaire (XQ) and MD Anderson Symptom Inventory for Head and Neck Cancer (MDASI-HN). Objective measures were unstimulated whole salivary flow rates (UWSFR) and stimulated salivary flow rates (SSFR). Patients were followed for 1 month after radiotherapy. XQ scores for acupuncture were significantly lower than sham controls starting in week 3 and lasted through the 1-month follow-up (all P's <0.001 except for week 3, which was 0.006), with clinically significant differences as follows: week 6 - RR 0.28 [95% confidence interval, 0.10, 0.79]; week 11 - RR 0.17 [95%CI, 0.03, 1.07]. Similar findings were seen for MDASI-HN scores and MDASI-Intrusion scores. Group differences for UWSFR and SSFR were not found. In this small pilot study, true acupuncture given concurrently with radiotherapy significantly reduced xerostomia symptoms and improved QOL when compared with sham acupuncture. Large-scale, multi-centre, randomised and placebo-controlled trials are now needed.
    European journal of cancer (Oxford, England: 1990) 01/2012; 48(11):1692-9. DOI:10.1016/j.ejca.2011.12.030 · 4.82 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In our previous study, the mouse double minute 2 (MDM2) was identified as one of the leading genes that promote the metastasis of pancreatic cancer (PC). However, the mechanism by which MDM2 promotes metastasis of PC is not understood. In this study, we show that down-regulation of MDM2 through lentivirus-mediated RNA interference could also suppress in vitro proliferation and in vivo tumor growth, and led to an obvious inhibition of both in vitro invasion and in vivo live metastases of SW1990HM cells which had an over-expression of MDM2 and a higher metastatic potential. Moreover, we also show that the down-regulation of MDM2 induced a significant decrease in MMP9, Ki-67 and increase in P53, E-Cadherin expression, and results in an altered expression of genes involved in metastasis, apoptosis, and cell proliferation. Our results suggest that MDM2 plays an important role in metastasis as well as tumor growth of PC. MDM2 could be a hopeful target for the control of PC.
    Molecular and Cellular Biochemistry 12/2011; 387(1-2). DOI:10.1007/s11010-011-1208-4 · 2.39 Impact Factor
  • Pancreas 10/2011; 40(7):1160-2. DOI:10.1097/MPA.0b013e318221816d · 3.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies based on epidemiological models published in this journal and elsewhere have demonstrated encouraging patterns suggesting that herbal treatment may improve prognosis in advanced colon and lung cancer patients. Various problems exist with data from nonrandomized studies of this type, but a strong signal of potential positive effect can be seen. The therapeutic mechanisms of traditional Chinese medicine in metastatic cancer are discussed against a hypothetical, dualistic antiproliferation model and immune-stimulation model of tumor progression and regression. Recommendations are made for a strategy to demonstrate more conclusively the efficacy of adjunct herbal treatment during cancer chemotherapy and for discussions with patients until such time as the efficacy trials are completed.
    Integrative Cancer Therapies 09/2011; 10(3):NP1-NP11. DOI:10.1177/1534735411421172 · 2.01 Impact Factor
  • Huiru Guo, Luming Liu, Jan P A Baak
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND. Traditional Chinese herbal medicine was associated with improved prognosis in patients with performance score 0-1 at the time of diagnosis of stage IV pulmonary adenocarcinoma (PAC) treated with platinum-based chemotherapy (PBT). OBJECTIVE. The authors investigated the effect of 1- to 4-month lag time to traditional Chinese medicine (TCM) treatment on the median and 1-year survival of PBT-PAC patients. The median lag time to treatment was 3 months. In the first 3 months, about 35% of the patients died, but thereafter the survival curve flattened off and the death of the next 35% to 40% of patients took 9 months. Leaving out patients with lag time up to 3 months therefore would be a reasonable choice. To be on the safe side, the effects of leaving out patients up to 4 months were investigated. The Kaplan-Meier survival curves were used. The median and 1-year survival of the PBT-PAC patients was 5.0 months and 27%, respectively. Leaving out patients with 0-1 month follow-up, 0-2, 0-3, and 0-4 months follow-up changed the median and 1-year survival, respectively, to 5.5 months and 32%, 6.5 months and 36%, 9.0 months and 43%, and 10.0 months and 52%. The median survival of PBT + TCM in PAC patients was 22.6 months and 78%. Median lag time to TCM treatment was 3.0 months. With up to 4 months lag time to treatment due to combined patients' and TCM doctor's waiting time, the improved survival of PBT + TCM performance score 0-1 (fully ambulant) patients at the time of diagnosis still is significant (P < .01, hazard ratio = 0.51). Moreover, the survival of patients treated by TCM doctors with little or more months lag time to treatment was not different (P = .79). Increasing lag time to treatment up to 4 months improves the median and 1-year survival of PBT patients without TCM but is unlikely to explain the greatly improved prognosis of PBT + TCM treated patients with fully ambulant stage IV PAC.
    Integrative Cancer Therapies 08/2011; 10(3):234-9. DOI:10.1177/1534735411418112 · 2.01 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Bufalin, a major bioactive component of the Chinese medicine Chansu, has been reported to exhibit significant antitumor activity against various cancer cell lines. However, the exact mechanism remains unclear. In this study, we demonstrated that bufalin inhibited the growth of hepatocellular carcinoma (HCC) cells in a dose-dependent manner, which correlated with the expression level of Na+/K+-ATPase α3 in HCC cells. The IC50 of bufalin markedly increased when Na+/K+-ATPase α3 was silenced by RNA interference. Furthermore, we show that bufalin increased the phosphorylation of Akt and ERK1/2 while inhibited FoxO3a expression. Thus, our study suggests that Na+/K+-ATPase α3 might serve as a therapeutic target for bufalin in HCC, and its expression status may help predict sensitivity of HCC cells to bufalin treatment.
    Oncology Reports 03/2011; 25(3):825-30. DOI:10.3892/or.2010.1120 · 2.19 Impact Factor

Publication Stats

242 Citations
90.23 Total Impact Points

Institutions

  • 2009–2015
    • Fudan University
      • • Department of Oncology
      • • Department of Statistics
      Shanghai, Shanghai Shi, China
  • 2011
    • University of Texas MD Anderson Cancer Center
      Houston, Texas, United States
  • 2009–2011
    • Northeast Agricultural University
      Charbin, Heilongjiang Sheng, China