Li Ma

Tianjin Medical University, T’ien-ching-shih, Tianjin Shi, China

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Publications (22)10.04 Total impact

  • Zhongguo fei ai za zhi = Chinese journal of lung cancer 07/2011; 14(7):617-9.
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    ABSTRACT: This study compared the efficacy and toxicities of cetuximab combined with chemotherapy versus chemotherapy for patients with metastatic colorectal cancer (mCRC). The influence of KRAS mutation status on the outcomes was also investigated. Literature retrieval, trials selection and assessment, data collection, and statistical analysis were performed according to the Cochrane Handbook 5.0.2. The outcome measures were tumor response rate, progression-free survival, overall survival, and adverse effects. Four randomized controlled trials, comprising totally 2,912 patients, were included. Meta-analysis showed higher response rate (RR 1.93; 95% CI, 1.14-3.26) and significant improvement in progression-free survival (PFS; HR 0.80; 95% CI, 0.67-0.95) in cetuximab-chemotherapy groups versus chemotherapy groups. There was no significant difference between the two treatment groups regarding overall survival (OS; HR 0.95; 95% CI, 0.87-1.05). In wild-type KRAS patients, treatment with cetuximab plus chemotherapy significantly increased response rate (RR 1.44; 95% CI, 1.20-1.73) and improved PFS (HR 0.64; 95% CI, 0.50-0.84), as compared with chemotherapy groups, but not for OS (HR 0.84; 95% CI, 0.64-1.11). In mutant KRAS patients, there was no significant difference between those treated with cetuximab plus chemotherapy and those with chemotherapy alone regarding response rate (RR 0.81; 95% CI, 0.61-1.08), PFS (HR 1.37; 95% CI, 0.81-2.31), and OS (HR 1.03; 95% CI, 0.74-1.44). The risk of grade 3/4 rash, diarrhea, neutropenia, and fatigue was significantly increased in cetuximab combination groups as compared with chemotherapy groups. The use of cetuximab in addition to chemotherapy was a valid alternative for patients with mCRC. Benefit of cetuximab was only limited to patients with wild-type KRAS tumors.
    International Journal of Colorectal Disease 04/2011; 26(8):1025-33. · 2.24 Impact Factor
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    ABSTRACT: To study on invasion and metastasis-associated genes of lung cancer related with NM23-H1 gene. Human gene expression chip based on the subtracted cDNA libraries was constructed. After microarray hybridization, clones sequencing, sequence homology search, the information of differently expressed genes in human large cell lung cancer cell line of L9981 and L9981-nm23-H1 were obtained and then further confirmed by real-time quantitative PCR. Gene expression profiling chips of differently expressed genes in human large cell lung cancer cell line L9981 and L9981-nm23-H1 were successfully constructed. After microarray hybridization, sequence homology search, 19 differentially expressed genes were observed. After real-time quantitative PCR evaluation, we found that the mRNA of 8 genes including PSMA7, SBDS, ODC1, YARS, CSDA, PTP4A1, SHPRH and TOMM7 was up-regulated in the cell line of L9981 after transfected with NM23-H1 gene, whereas the mRNA of PKM2 and GMNN was down-regulated. NM23-H1 gene may be the upstream regulator of metastasis-associated genes, which can regulate the downstream genes to achieve a series of lung cancer metastatic potential.
    Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 11/2010; 41(6):941-5.
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    ABSTRACT: As a tumor metastasis suppressor gene, the functions of nm23-H1 gene are still unclear. The aim of this study is to better understand the mechanism of lung cancer metastasis and to find new biomarkers for early diagnosis and new target for therapy by conducting comparative proteomics between the human high-metastatic large cell lung cancer cell lines (L9981) and L9981-nm23-H1 (constructed with transfecting nm23-H1 gene into the L9981 cell line). The total proteins of L9981 and L9981-nm23-H1 were separated by immobilized pH gradient (IPG)-based 2-dimensional electrophoresis (2-DE); the significantly differently expressed proteins were examined by mass spectrometry and analyzed by bioinformatics. It was observed that nm23-H1 gene transfection caused remarkable changes of the proteome of L9981 compared with L9981-nm23-H1 cells: 5 proteins were deleted, 9 proteins appeared, 16 proteins downregulated, and 12 proteins up-regulated. These proteins are involved in cell framework, signal transduction, metabolism, proliferation and metastasis. After nm23-H1 gene is transfected into L9981, proteome in L9981 is remarkably changed. These changes of the proteome could serve as a basis for reversing the invasive and metastatic phenotype in lung cancer and elucidating the mechanisms of the metastasis of lung cancer.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 10/2010; 13(10):928-32.
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    ABSTRACT: Introduction:  An increasing number of studies have proven that the kinase suppressor of Ras (KSR1) functions as a scaffolding protein that coordinates the assembly of a multiprotein complex containing mitogen-activated protein kinase and its upstream regulators. However, a few studies have reported that KSR1 can activate c-Raf-1. Therefore, whether KSR1 possesses a kinase activity has been an unresolved issue until now.Materials and Methods:  pCMV-Tag2b-KSR plasmids were transfected into 293T cells. In vitro autophosphorylation was assayed by autoradiography and in vitro kinase was assayed by reversed-phase high performance liquid chromatography.Results:  We observed that wild-type KSR1 (WT-KSR) and N-terminal KSR1 (N-KSR) were phosphorylated, but the C-terminal KSR1 (C-KSR) and vector proteins were not. The high performance liquid chromatography profile showed not only the adenosine diphosphate peak but also the uridine triphosphate peak in the WT-KSR and N-KSR groups; both peaks were considerably more significant in these groups than in the others. The WT-KSR and N-KSR groups exhibited transphosphorylation and autophosphorylation activities, while the other groups revealed almost no activity.Discussion:  Here, we demonstrate the nucleoside diphosphate kinase activity of the KSR1 complex and that this activity can be independent of the C-terminus of KSR1. Additionally, we found the autophosphorylation activity of the KSR1 complex to be extremely weak, suggesting that the KSR1 complex possesses an extremely weak kinase activity irrespective of whether it is nucleoside diphosphate kinase activity or serine/threonine protein kinase activity. These data suggest that the kinase activity of the KSR1 complex is derived from its associated proteins.
    Thoracic Cancer. 09/2010; 1(3):109 - 115.
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    ABSTRACT: Skeletal metastase is one of the most common complications related to advanced cancer. The aim of this study is to analyze the effectiveness and safety of radiotherapy plus intravenous bisphosphonates versus radiotherapy alone for treating bone metastasis. We searched the Cochrane Library, PubMed, EMBASE, CBM, CNKI and VIP, as well as the reference lists of reports and reviews. The quality of included trials was evaluated by the Cochrane Handbook. Data were extracted and evaluated by two reviewers independently. The Cochrane Collaboration's Rev-Man 5.0 was used for data analysis. Twenty-two trials involving 1 585 patients were included. Compared with radiotherapy alone, radiotherapy plus intravenous bisphosphonates was more effective in total effective rate of pain relive (RR = 1.21, 95% CI: 1.13-1.30, P < 0.001), average abated time (WMD = 16.00, 95% CI: 10.12-21.88, P < 0.001), and quality of life (RR = 1.25, 95% CI: 1.08-1.45, P = 0.003, with significant differences. Side effects have no significant differences between the two groups except fever (RR = 5.61, 95% CI: 3.11-10.13, P < 0.001). Current evidence supports more effective of radiotherapy plus intravenous bisphosphonates for bone metastases. The combine treatment is safe and effective.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 05/2010; 13(5):533-9.
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    ABSTRACT: Cisplatin (DDP) plus vinorelbine (NVB) constitute the first-line regimen (NP regimen) for non-small cell lung cancer (NSCLC). Oxaliplatin (OXA) is another effective drug in treatment of NSCLC with mild toxicities to gastrointestinal tract, kidney and bone marrow. The aim of this study is to evaluate the efficiency and safety between NVB plus OXA (NO) regimen and NP regimen for advanced NSCLC. We searched CBM CNKI, VIP, Cochrane Library, PubMed, EMBASE, ASCO etc. conference proceedings and internet information. Randomized controlled trials of NO versus NP for advanced NSCLC were included; we evaluated the quality of the included studies and analyzed data by Cochrane Collaboration's RevMan 5.0 software. Fourteen randomized trials involving 1 270 patients were included. There were no statistical differences between NO and NP in overall response rate, disease control rate, 1-year survival rate, anemia and thrombocytopenia. Gastrointestinal toxicity, leucopenia, alopecia and kidney toxicity were more serious in NP (P < 0.05), but neuritis was more serious in NO, with significant difference (P < 0.05). The clinical efficacy of NO and NP for advanced NSCLC was similar, but the side effects were different. The toxicity of NO has the tendency to be more tolerable.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 02/2010; 13(2):112-7.
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    ABSTRACT: To study the expression of the Syk (Spleen Tyrosine Kinase) gene and methylation in its promoter region in lung cancer. To investigate the relationship between silencing of the Syk gene and DNA methylation of the Syk promoter region. RT-PCR (Semi-quantitative reverse transcription PCR), Real-time PCR (Real-time quantitative PCR) and immunohistochemistry technique, the expression of Syk in specimens from 3 lung cancer cell lines and 16 lung cancer patients (tumor tissues and adjacent normal tissues). MSP (Methylation-specific PCR) was used to analyze the methylation status of the Syk promoter region. Then we also investigated the role of restoring Syk expression by using a DNA methyltransferase inhibitor, 5-aza-CdR (5-aza-2'-deoxycytidine), in suppressing invasion of lung cell lines. No expression of the Syk gene was detected in the 3 lung cancer cell lines. In the 16 lung patient samples, Syk expression was significantly lower in the tumor tissues than in the adjacent normal tissues (P < 0.05). Consistently, immunohistochemistry analyses of Syk protein expression showed that in the cancer tissues Syk protein expression accounted for 5% (1/20), and in the adjacent normal tissues the rate of expression was 100% (20/20). The correlation was highly significant (chi2 = 36.19, P < 0.005). In the only case that showed a positive expression of cancer textus, the level was inferior to the adjacent tissue. In the two lung cancer cell lines (L9981, A549) that lack the endogenous Syk epression, 4uM demethylation agent 5-aza-CdR treatment was able to reactivate the Syk gene expression. Hypermethylation leads to silencing of the Syk gene in human lung carcinoma. Methylation of the Syk promoter and loss of Syk expression in lung cancer are independent biomarkers, a determination which may offer guidance for selecting appropriate diagnoses and treatments. Syk may be a potential tumor suppressor in human lung cancer.
    Clinical laboratory 01/2010; 56(9-10):407-16. · 0.92 Impact Factor
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    ABSTRACT: Nuclear factor erythroid-2 related factor 2 (Nrf2) is a key transcription factor in oxidation-reduction reaction. It has been proved that Nrf2 is relevant to cisplatin-resistance in ovarian cancer cells. Up to now, little is know whether Nrf2 and it's signal patheways play an important role in cisplatin-resistance in pulmonary adenocarcinoma cells or not. The aim of this study is to explore the expression levels of transcription factor Nrf2 and its target genes in A549 cells which are resistance to cisplatin and reveal the mechanism behind it. A549/DDP and A549 were cultured in vitro. MTT was used to detect the drug resistance index of A549/DDP cells. Real-time PCR was used to evaluate the expression of transcription factor Nrf2 and its target genes mRNA. The drug resistance index of A549/DDP was 12.12, and its Keap1, Nrf2, NQO1, GSTP1, GCL, HO-1, MRP4 mRNA expressions were all significantly increased compared with A549 (P<0.01). On the other hand, MRP1, MRP2, MRP3 showd the crosscurrent (P<0.01). It proves that the transcription factor Nrf2 and it's signal pathways are closely related with drug resistance of tumors. Moreover, this provides a new direction to reverse drug resistance and have significance to avoid and overcome drug resistance of tumor.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 11/2009; 12(11):1150-4.
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    ABSTRACT: The Phosphorylation is the key activity of nm23-H1. The aim of this study is to explore the effect of different amino acid mutation on the phosphorylation status of nm23-H1. The wild type nm23-H1 was as the control of this study. Autoradiography was used for detecting the serine and histidine autophosphorylation of wild type (WT) and mutant nm23-H1 (P96S, H118F, S120G and S44A); RP-HPLC was used for detecting the NDPK activity of above proteins. The autophosphorylation activities of serine and histidine from high to low were P96S, WT, S44A, S120G and H118F, respectively, while the NDPK activities from high to low were WT, S120G, P96S, S44A, H118F. A highly positive correlation was found between serine and histidine autophosphorylation activity of above proteins (r =0.985, P <0.01), but no significant correlation was found between NDPK and serine or histidine autophosphorylation activity (r=0.458, P >0.05, and r =0.482, P >0.05, respectively). Site mutation of nm23-H1 can affect the phosphorylation activity. H118 site was the key amino acid of kinase activity, P96 site maybe related to phosphotransferring, S120 was the site of histidine autophosphorylation and serine autophosphorylation, while the S44 site may be another amino acid which possessed NDPK activity.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 03/2009; 12(3):193-7.
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    ABSTRACT: Nm23-H1 is a metastasis-suppressor gene. However, its molecular mechanism of suppressing metastasis is unknown until now. The aim of this study is to construct prokaryotic expression vector of wild and mutant type of nm23-H1 (WT, P96S, H118F), and then express and purify the proteins. wild and mutant type of nm23-H1 fragments were amplified by PCR. The prokaryotic expression vectors of pET28anm23-H1 were constructed by gene recombination technique and verified by restriction enzyme analysis and sequencing. The positive clones were transformed into E. coli BL21 (DE3) and soluble analysis of the expression was conducted in this system. The proteins were purified by nickel column chromatography and identified by Western blot The sequences and open read frames of all the pET28a-nm23-H1 plasmids were completely correct. After transforming, these plasmids can express the target proteins. The protein production was very high, and all the proteins were soluble expression. The molecular weight of wild and mutant type of nm23-H1 was 20 kDa detected by Western blot, which was as the same as the objective protein. We have succeeded in constructing the prokaryotic expression vectors of pET28a-nm23-H1 (WT, P96S, H118F) and the proteins which expressed can be used in following studies.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 01/2009; 12(1):23-7.
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    ABSTRACT: It has been confirmed that nm23-H1 gene is one of the tumor metastasis suppressor genes. Up to now, the exact mechanism of nm23-H1 gebe is uncertain. The aim of this study the mechanism of metastasis suppressor gene nm23-H1 involving in the Ras signaling of lung cancer. The wild and mutant type of pEGFP-nm23-H1 plasmids [WT (wild type), H118F, S120G, P96S, S44A] were transfected into the L9981 lung cancer cell lines through liposome method, and the complex of KSR and nm23-H1 was detected through co-immunoprecipitation and Western blot assay. The human KSR could be detected in the nm23-H1 immunoprecipitations in all the trasfected L9981 lung cancer cell lines. But no significant difference of KSR expression was found in the wild and mutant nm23-H1 trasfected cell lines (F =0.190, P =0.938). There was a close interaction between nm23-H1 and KSR, which was independent of the nm23-H1 mutation. Nm23-H1 involving in the Ras signaling of lung cancer may be through the KSR gene.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 10/2008; 11(5):700-3.
  • Zhongguo fei ai za zhi = Chinese journal of lung cancer 10/2008; 11(5):742-6.
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    ABSTRACT: It has been proven that nm23-H1 gene is an important metastaticsuppressed gene of lung cancer. In order to screen the differential expression genes related to nm23-H1 , we constructed the suppression subtractive cDNA libraries of human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene by suppression subtractive hybridization (SSH) in this study, which lay a solid foundation for further screening and cloning metastatic-related genes of nm23-H1. The forward and reverse suppression subtractive cDNA libraries were constructed in the human large cell lung cancer line L9981 before and after transfection with nm23-H1 gene (L9981 and L9981-nm23-H1) by SSH method. The positive clones were preliminarily screened by bluewhite colony, and precisely identified by PCR. The suppression subtractive cDNA libraries were successfully constructed in the human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene (L9981-nm23-H1 and L9981). After the blue-white screening, about three hundred positive clones in the forward subtracted library and four hundred positive clones in the reverse subtracted library were obtained. Ramdom analysis of 96 clones in each library with colony PCR methods showed that 84 clones in the forward subtracted library and 83 clones in the reverse subtracted library contained (300-750) bp inserts. SSH is proved to be an efficient tool for differential expression gene cloning. The forward and reverse suppression subtractive cDNA libraries of human large cell lung cancer line L9981 transfected and untransfected with nm23-H1 gene (L9981-nm23-H1 and L9981) are successfully constructed by SSH and T/A cloning technology. The expression of nm23-H1 gene in the human large cell lung cancer cell lines may affect the differential expression of some metastatic-related genes.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 08/2008; 11(4):482-8.
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    ABSTRACT: An abstract is unavailable. This article is available as HTML full text and PDF.
    Journal of Thoracic Oncology 07/2007; 2(8):S496. · 4.47 Impact Factor
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    ABSTRACT: The Nm23-H1 gene is a metastasis suppressor gene. However, its biochemical mechanism of suppressing the metastatic potential of cancer cells is still unknown. The previous hypothesis that a histidine protein kinase activity may contributes to the motility-suppressive effect of Nm23-H1 could not explain why the H118F mutant, a kinase-deficient mutant, still had motility-suppressive ability. We conducted a study on the double mutant P96S/S120G of Nm23-H1 and succeeded in introducing the RP-HPLC method in NDPK assay. The results showed that the double mutant P96S/S120G, when expressed in the bacteria, was completely aggregated in inclusion bodies; this mutant abrogated not only its motility-suppressive ability, but also its NDPK activity. Based on previous work and this study, we prompted that the deficiency of motility-suppressive function of S120G, P96S, and P96S/S120G mutants was due to their altered structure, which might deprive Nm23-H1 of most activities including kinase activity or interactions with other proteins.
    Biochemical and Biophysical Research Communications 06/2007; 356(2):348-53. · 2.41 Impact Factor
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    ABSTRACT: Screening metastatic-related genes of lung cancer is helpful to understand the molecular mechanisms of lung cancer invasion and metastasis. In order to screen the differential expression genes related to metastasis of lung cancer, we constructed and preliminarily screened the subtracted cDNA libraries of human large cell lung cancer cell lines with different metastatic potentials in this study. Subtracted cDNA library was constructed in the different metastastic potential cell lines NL9980 and L9981 by suppression subtractive hybridization (SSH) method. The positive clones were preliminarily screened by blue-white colony based on the α-complementary principal, and precisely identified by PCR. The forward and reverse subtracted libraries were screened and identified by dot blot to obtain the clones corresponding to differential expression segments. The subtracted cDNA libraries were successfully constructed in the different metastastic potential cell lines NL9980 and L9981. Three hundred and seven positive clones in the forward subtracted library and 78 positive clones in the reverse subtracted library were obtained by the dot blot method. SSH is proved to be an efficient tool for differential expression gene cloning. The forward and reverse subtracted cDNA libraries of different metastastic potential cell lines are constructed by this method. The differential expression genes related to tumor metastasis might exist in the human large cell lung cancer cell lines with different metastasis potential.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 06/2007; 10(3):163-7.
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    ABSTRACT: Lung cancer is one of the most malignant cancers which is hazarding the people's health and life in the world. At present, it is a highlight to exploit antitumor drug from plant at home and abroad. The aim of this study is to observe the effects of polysaccharid (PS-T) on expression of angiogenic-related gene mRNA in human high-metastatic large cell lung cancer cell line L9981, and to explore its possible molecular mechanism. L9981 in vitro was cultured, and the growth data were obtained by trypan blue staining. The mRNA transcript expression of β-catenin, E-cadherin, TIMP-1, CD44V6, MMP-2, endostatin, VEGF was detected in L9981 by RT-PCR before and after treating with PS-T. The ability of invasion of L9981 was determined by Boyden chamber method. (1)PS-T had remarkably inhibitive effects on the growth of L9981 in vitro. The inhibitive rate of PS-T on L9981 was concentration-dependent. No significant difference of inhibitive rate was found among the PS-T (1g/L), cisplatin (3mg/L) and PS-T (0.05g/L) + cisplatin (1.5mg/L)(P > 0.05). (2)The mRNA expression level of β-catenin, E-cadherin, TIMP-1, endostatin and MMP-2 was upregulated, while that of VEGF and CD44V6 was downregulated. Out of them the mRNA expression level of TIMP-1 and endostatin was remarkably upregulated, the expression level of CD44V6 was significanyly downregulated. (3)The in vitro invasive abilities of L9981 was significantly decreased in the PS-T, DDP and PS-T+DDP groups compared with that in blank control group. (1)PT-S could inhibit the growth of human high-metastatic large cell lung cancer cell line L9981 in vitro, the effect is dose-dependent. (2)PS-T can down- or up-regulate the mRNA transcript expression of some angiogenic-related gene mRNA. (3)PS-T has remarkably coordinating effects with cisplatin in the L9981 lung cancer cell line.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2006; 9(2):137-42.
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    ABSTRACT: The present experimental data have showed that the function of kinase suppressor of Ras (KSR) is mainly as a scaffold protein that coordinates the assembly of a multiprotein complex containing MAPK and its upstream regulators. But whether KSR has kinase activity is still the point of argument until now. The aim of this study is to construct eukaryotic expression vectors of carboxyl terminus and amino terminus of KSR and to detect their expression in 293T cell line. N-KSR and C-KSR were amplified by PCR. The eukaryotic expression vectors of pCMV-Tag2b-N-KSR and pCMV-Tag2b-C-KSR were constructed by gene recombination technique and the recombinant plasmids were verified by restriction enzyme analysis and sequencing. Then positive clones were transfected into 293T cell line. Expression of target proteins was analyzed by Western blot. The sequences and open read frames of the two vectors were both completely concordant with experiment design. The target proteins could be observed in transfected 293T cells by Western blot. Eukaryotic expression vectors of pCMV-Tag2b-N-KSR and pCMV-Tag2b-C-KSR are successfully constructed, and they can be expressed in 293T cells. It provides an experimental base for further research work.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2006; 9(2):123-6.
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    ABSTRACT: It has been proved that selenium has remarkable effects in the prevention of cancer and proliferation inhibition for breast cancer and prostate cancer. Up to now, little is known, however, if methylseleninic acid (MSA) has the anticancer effect on lung cancer or not. The objective of this study is to detect the effect of MSA on proliferation inhibition and apoptotic induction for human high-metastatic large cell lung cancer cell line L9981, and to explore the molecular mechanisms. The changes of proliferation, clone formation, apoptotic level and cell cycles were detected in L9981 by trypan blue staining, clone formation suppression test, and flow cytometry before and after treating with different concentration of MSA. The expression level of proliferative-related and apoptotic-related genes was also determined in L9981 by flow cytometry. (1)The proliferation ability of L9981 was remarkably inhibited at the concentration of 0.5μmol/L of MSA (P < 0.05), and the cells were arrested at G0/G1 phase after treating with the same concentration. (2)Apoptosis of L9981 was remarkably induced by MSA at the concentration of 2.5μmol/L (P < 0.05). (3)The clone formation ability of L9981 was significantly suppressed by MSA at the concentration of 5.0μmol/L (P < 0.05). (4)The expression levels of P53, P21, Fas, FasL and Bax were remarkably up-regulated after treatment with MSA. (1)MSA can significantly suppress the proliferation and clone formation ability of human high-metastatic large cell lung cancer cell line L9981, and also induce apoptosis of L9981. (2)The anticancer effects of MSA might be related to regulate the expression of cell cycle-related genes and apoptotic-related genes in the human high-metastatic large cell lung cancer line L9981.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2006; 9(2):103-8.

Publication Stats

25 Citations
10.04 Total Impact Points

Institutions

  • 2008–2011
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China
  • 2010
    • Third Military Medical University
      Ch’ung-ch’ing-shih, Chongqing Shi, China
  • 2009–2010
    • Tianjin Medical University Cancer Institute and Hospital
      T’ien-ching-shih, Tianjin Shi, China
  • 2006–2008
    • Sichuan University
      • State Key Laboratory of Biotherapy
      Chengdu, Sichuan Sheng, China