Yening Jin

Ruijin Hospital North, Shanghai, Shanghai Shi, China

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Publications (8)33.14 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: The purposes of this study were to determine the expression profiles of microRNA-34a (miR-34a) in human gastric cancer cell line (SGC-7901) and cisplatin-resistant cell lines (SGC-7901/DDP), and to establish the correlation between miR-34a expression profile and the sensitivity of human gastric cancer cell to cisplatin-based pattern, thereby providing new methods and strategies for treating gastric cancer. Gastric cancer cell line (SGC-7901) and cisplatin-resistant cell line (SGC-7901/DDP) were cultivated in vitro, respectively. Quantitative real-time PCR (qRT-PCR) and Western blot were utilized to determine the expression profiles of miR-34a and survivin in both gastric cancer cell lines. With miR-34a mimic and miR-34a inhibitor transfected into SGC-7901 and SGC-7901/DDP for 48 h, post-transfection changes of miR-34a expression was determined; the effects of miR-34a ectopic expression on the viability of cisplatin-induce gastric cancer cell were assayed by the MTT method. The effects of miR-34a ectopic expression on apoptosis of cisplatin-induce gastric cancer cell were determined by Annexin V/propidium iodide (PI) double staining method and flow cytometry. The effects of miR-34a ectopic expression on the AKT and p-AKT expression of cisplatin-induce gastric cancer cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin. As shown by qRT-PCR and Western blot analyses, the expression of miR-34a in cisplatin-resistant cell lines decreased significantly in comparison to that of SGC-7901 cell line (p < 0.05), while significant up-regulation of survivin expression was also observed (p < 0.05). Compared with the control group, the expression of miR-34a increased significantly in SGC-7901 cells transfected with miR-34a mimic for 48 h (p < 0.01). After miR-34a inhibitor transfection, the expression of miR-34a decreased significantly (p < 0.05). The viability of cisplatin-induce gastric cancer cells increased significantly (p < 0.05) with significant decrease of apoptosis after miR-34a expression inhibition, as demonstrated by MTT and flow cytometry with miR-34a over-expression, the viability of cisplatin-induce gastric cancer cells decreased significantly (p < 0.05), with significant apoptosis increase (p < 0.05). As shown by Western blot and flow cytometry, in comparison to the control group, Wortmannin could inhibit miR-34a inhibitor and DDP induced up-regulation of p-AKT significantly (p < 0.05) and stimulated apoptosis. In conclusion, miR-34a expression was down-regulated in cisplatin-resistant cell lines. miR-34a over-expression could improve the sensitivity of gastric cancer cells against cisplatin-based chemotherapies, with PI3K/AKT/survivin signaling pathway possibly involved in the mechanism.
    Tumor Biology 09/2013; · 2.52 Impact Factor
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    ABSTRACT: Abstract Objective: To report the feasibility of laparoscopic resection with intraoperative radiotherapy for local advanced rectal cancer in an Asian man. Patient and Methods: A 55-year-old man with adenocarcinoma of the rectum presented at Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China. The tumor, with a size of 5×5 cm, was located 3 cm from the anus and covered a circular area around approximately two-thirds of the bowel. The carcinoembryonic antigen level was 29.86 ng/mL; a nodule was detected, but no distant metastasis was detected. Preoperative staging was T4N1M0. After the patient signed the consent form, laparoscopic resection with intraoperative radiotherapy was performed. Results: The operation time was about 180 minutes, intraoperative blood loss was 100 mL, and postoperative hospital stay was 8 days. The patient had no postoperative complications. Conclusions: Performance of laparoscopic resection with intraoperative radiotherapy for local advanced rectal cancer is feasible in selected patients.
    Journal of Laparoendoscopic & Advanced Surgical Techniques 12/2012; · 1.07 Impact Factor
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    ABSTRACT: We aimed to investigate the expression of microRNA-34a (miR-34a) in human gastric cancer cells and to evaluate the effects of miR-34a, acting via its gene survivin, on gastric cancer cell HGC-27 to provide potential new strategies for treating gastric cancer. In vitro cultures of the human gastric cancer cell lines MGC80-3, HGC-27, NCI-N87, and SGC-7901 and the normal human gastric epithelial cell line GES-1 were established. The expression of miR-34a in each gastric cancer cell line and GES-1 normal human gastric epithelial cell line was detected using quantitative real-time polymerase chain reaction (qRT-PCR). After the HGC-27 cells were transfected with a miR-34a mimic for 48 h, the changes in the expression levels of miR-34a were detected using qRT-PCR. The effect of miR-34a on HGC-27 cell viability was measured using a tetrazolium-based colorimetric [-(4,5)-dimethylthiahiazo-(-z-y1)-3,5-di-phenytetrazoliumromide (MTT)] assay. Flow cytometry was used to analyze the effects of miR-34a on HGC-27 cell proliferation. Annexin V/propidium iodide double staining and flow cytometry were used to analyze the effects of miR-34a on HGC-27 cell apoptosis. A Transwell invasion chamber was used to detect the effects of miR-34a on HGC-27 cell invasion. Finally, western blotting was used to analyze the effects of miR-34a on survivin protein expression. The qRT-PCR test determined that miR-34a expression in gastric cancer cells was significantly reduced compared to the normal gastric epithelial cell line GES-1 (p < 0.01). Compared to the control group, cellular miR-34a expression levels were significantly increased in HGC-27 human gastric carcinoma cells after transfection with a miR-34a mimic for 48 h (p < 0.01). The MTT assay demonstrated that after overexpressing miR-34a in HGC-27 cells, cellular viability was significantly reduced (p < 0.05). Flow cytometry analysis determined that upon miR-34a overexpression, the proliferation index decreased significantly (p < 0.05), and cellular apoptosis was significantly increased (p < 0.01). The Transwell invasion chamber assay illustrated that after increasing the expression of miR-34a, the number of cells passing through the Transwell chamber was significantly reduced (p < 0.01). Based on western blotting, compared with the control group, survivin protein expression levels were significantly decreased in the HGC-27 cells transfected with the miR-34a mimic for 48 h (p < 0.01). In conclusion, the expression level of miR-34a was downregulated in human gastric cancer cell lines. miR-34a can negatively regulate survivin protein expression and inhibit gastric cancer cell proliferation and invasion. Therapeutically enhancing miR-34a expression or silencing the survivin gene may benefit patients with gastric cancer.
    Tumor Biology 12/2012; · 2.52 Impact Factor
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    ABSTRACT: The present study was designed to investigate the clinicopathological role of survivin-expressing circulating tumor cells (CTCs) and to determine whether the presence of survivin-expressing CTCs is an independent predictor of tumor recurrence following curative resection of gastric cancer. This study included 98 patients who underwent potentially curative resection. Reverse transcription polymerase chain reaction enzyme linked immunosorbent assay (RT-PCR ELISA) was used to measure survivin mRNA in peripheral blood. Of the 98 patients studied, 45 (45.9%) were positive for survivin mRNA. Survivin mRNA expression correlated with Lauren classification (P < 0.001), pathological tumor (pT) stage (P < 0.001), pathological tumor node metastasis (pTNM) stage (P = 0.009), and degree of differentiation (P = 0.001). The pTNM stage and the status of survivin mRNA were independent prognostic factors of disease-free survival (P = 0.007 and <0.001, respectively). The detection of CTCs expressing survivin mRNA could be a good clinical biomarker used to predict the prognosis of patients with curatively resected gastric cancer.
    Journal of Surgical Oncology 02/2011; 103(2):110-5. · 2.64 Impact Factor
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    ABSTRACT: Patients with glioblastoma multiforme, the most aggressive form of glioma, have a median survival of approximately 12 months. Calcium (Ca(2+)) signaling plays an important role in cell proliferation, and some members of the Ca(2+)-permeable transient receptor potential canonical (TRPC) family of channel proteins have demonstrated a role in the proliferation of many types of cancer cells. In this study, we investigated the role of TRPC6 in cell cycle progression and in the development of human glioma. TRPC6 protein and mRNA expression were assessed in glioma (n = 33) and normal (n = 17) brain tissues from patients and in human glioma cell lines U251, U87, and T98G. Activation of TRPC6 channels was tested by platelet-derived growth factor-induced Ca(2+) imaging. The effect of inhibiting TRPC6 activity or expression using the dominant-negative mutant TRPC6 (DNC6) or RNA interference, respectively, was tested on cell growth, cell cycle progression, radiosensitization of glioma cells, and development of xenografted human gliomas in a mouse model. The green fluorescent protein (GFP) and wild-type TRPC6 (WTC6) were used as controls. Survival of mice bearing xenografted tumors in the GFP, DNC6, and WTC6 groups (n = 13, 15, and 13, respectively) was compared using Kaplan-Meier analysis. All statistical tests were two-sided. Functional TRPC6 was overexpressed in human glioma cells. Inhibition of TRPC6 activity or expression attenuated the increase in intracellular Ca(2+) by platelet-derived growth factor, suppressed cell growth and clonogenic ability, induced cell cycle arrest at the G2/M phase, and enhanced the antiproliferative effect of ionizing radiation. Cyclin-dependent kinase 1 activation and cell division cycle 25 homolog C expression regulated the cell cycle arrest. Inhibition of TRPC6 activity also reduced tumor volume in a subcutaneous mouse model of xenografted human tumors (P = .014 vs GFP; P < .001 vs WTC6) and increased mean survival in mice in an intracranial model (P < .001 vs GFP or WTC6). In this preclinical model, TRPC6 channels were essential for glioma development via regulation of G2/M phase transition. This study suggests that TRPC6 might be a new target for therapeutic intervention of human glioma.
    CancerSpectrum Knowledge Environment 07/2010; 102(14):1052-68. · 14.07 Impact Factor
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    ABSTRACT: The aim of this study was to assess the efficacy and toxicity of the combination of paclitaxel and nedaplatin as a first-line chemotherapy for patients with advanced esophageal cancer. Patients with advanced esophageal cancer received 175 mg/m(2) of paclitaxel over a 3 h infusion, followed by nedaplatin 80 mg/m(2) in a 1 h infusion on day 1 every 3 weeks until the documented disease progression, unacceptable toxicity or patient's refusal. Between March 2005 and December 2007, 48 patients entered in the study. Forty-six (95.8%) of the 48 patients were assessable for response. The overall response rate was 41.7% (95% CI, 27.8-55.7%) with 2 complete responses and 18 partial responses. The median follow-up period was 20.5 months (range, 12.5-27.2 months). The median overall time to progression and overall survival (OS) were 6.1 months (95% CI, 4.8-7.4 months) and 11.5 months (95% CI, 9.1-13.9 months), respectively. The estimate of OS at 12 and 24 months was 43.8% (95% CI, 29.7-77.8%) and 10.4% (95% CI, 1.8-19.1%), respectively. Most patients experienced anemia, during their course of therapy with 6 (13.0%) patients for grade 3/4 anemia, and grade 1 or 2 anemia was detected in 23 (50%) patients. Grade 3 leucopenia, neutropenia and thrombocytopenia were documented in 8 (17.4%), 9 (17.4%) and 2 (4.3%) patients, respectively. Grade 3 nausea and vomiting were detected in 3 (6.5%) and 2 (4.3%) patients, respectively. Two patients (4.3%) were hospitalized because of treatment-related complications. The treatment was well tolerated and no toxic death occurred. Combination of paclitaxel and nedaplatin is a tolerated treatment modality with promising activity in previously untreated advanced esophageal cancer.
    Japanese Journal of Clinical Oncology 07/2009; 39(9):582-7. · 1.90 Impact Factor
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    ABSTRACT: Channels formed by the canonical transient receptor potential (TRPC) subfamily of proteins are Ca(2+)-permeable, nonselective cation channels with various functions. Through a phospholipase C (PLC)-dependent mechanism TRPC6, a member of TRPC subfamily, can be activated by receptor tyrosine kinases (RTK) or G protein-coupled receptors (GPCR), which are implicated in cell proliferation and human malignancies. Here, we report that TRPC6 has a critical role in human gastric cancer development. Expression of TRPC6 was greatly upregulated in human gastric cancer epithelial cells compared with that in normal gastric epithelial cells. Treatment of AGS or MKN45 cells, human gastric cancer cell lines, with SKF96365, an agent known to inhibit TRPC channels, arrested cell cycle in G2/M phase and suppressed cell growth. Importantly, expressing a dominant negative mutant of TRPC6 (DNC6) in these cells also arrested cell cycle in G2/M phase and inhibited cell growth. The Ca(2+) elevation in the MKN45 cells evoked by histamine was inhibited by SKF96365 and DNC6. Moreover, inhibition of TRPC6 suppressed the formation of gastric tumors in nude mice. These results suggest that Ca(2+) elevation regulated by TRPC6 channels is essential for G2/M phase transition and for the development of gastric cancers.
    International Journal of Cancer 06/2009; 125(10):2281-7. · 6.20 Impact Factor
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    ABSTRACT: The efficacy of chemotherapy for advanced gastric cancer with palliative intent compared with supportive care alone is now widely accepted. However, the best choice of chemotherapy regimen for patients with advanced gastric cancer is still a matter of controversy and requires further investigation. This study is performed to evaluate the efficacy and safety of the FOLFOXIRI regimen (oxaliplatin 85 mg/m as a 2-h intravenous infusion, irinotecan 165 mg/m as a 90-min infusion, leucovorin 200 mg/m as a 2-h infusion, 5-fluorouracil 3200 mg/m as a 48-h continuous infusion on day 1, every 2 weeks) as first-line treatment for advanced gastric cancer. Forty-seven (95.9%) of the 49 patients were assessable for response. Two cases of complete response and 29 cases of partial response were confirmed, giving an overall response rate of 63.3% [95% confidence interval (CI): 49.8-76.8%]. The median time to progression and overall survival for all patients were 7.3 months (95% CI: 6.0-8.6 months) and 11.9 months (95% CI: 9.4-14.4 months), respectively. The estimate of overall survival at 12 months was 42.9% (95% CI: 29.0-56.7%). Most patients experienced neutropenia during their course of therapy with 49% of patients (n=23) for grade 3/4 neutropenia. Grade 3 nausea/vomiting, stomatitis, and diarrhea were observed in 20 (42.6%), two (4.3%), and five (10.6%) patients, respectively. Yet, no grade 4 nonhematologic toxicity was observed. The FOLFOXIRI combination is a tolerated treatment modality with promising activity in previously untreated advanced gastric cancer patients.
    Anti-cancer drugs 02/2009; 20(4):287-93. · 2.23 Impact Factor

Publication Stats

65 Citations
361 Views
33.14 Total Impact Points

Institutions

  • 2009–2011
    • Ruijin Hospital North
      Shanghai, Shanghai Shi, China
    • Shanghai Ruijin Hospital
      Shanghai, Shanghai Shi, China