MiR-133a induces apoptosis through direct regulation of GSTP1 in bladder cancer cell lines

Uchida, Youhei; Chiyomaru, Takeshi; Enokida, Hideki; Kawakami, Kazumori; Tatarano, Shuichi; Kawahara, Kazuya; Nishiyama, Kenryu; Seki, Naohiko; Nakagawa, Masayuki

doi:10.1016/j.urolonc.2010.09.017

Cited by 82 publications

(72 citation statements)

References 36 publications

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“…In current study statistically significant downregulation of GSTP1 was observed in brain tumor samples compared to control samples. Similar results have also been observed in breast cancer (Erlap et al, 2013), prostate cancer (Okino et al, 2007;Re et al, 2011) and colon cancer (Ritchie et al, 2009).Whereas conflicting results for GSTP1 expression pattern have been reported in some of other studies (Masood et al, 2011;Uchida et al, 2013). In present study, significant down-regulation of GSTP1 was observed in more advance grade of brain tumor samples when compared with early grade of brain tumor.…”

Section: Discussionsupporting

confidence: 88%

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Wahid¹,

Mahjabeen²,

Baig³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Most of the exogenous and endogenous chemical compounds are metabolized by enzymes of xenobiotic processing pathways, including the phase I cytochrome p450 species. Carcinogens and their metabolites are generally detoxified by phase II enzymes like glutathione-S-transferases (GST). The balance of enzymes determines whether metabolic activation of pro-carcinogens or inactivation of carcinogens occurs. Under certain conditions, deregulated expression of xenobiotic enzymes may also convert endogenous substrates to metabolites that can facilitate DNA adduct formation and ultimately lead to cancer development. In this study, we aimed to test the association between deregulation of metabolizing genes and brain tumorigenesis. The expression profile of metabolizing genes CYP1A1 and GSTP1 was therefore studied in a cohort of 36 brain tumor patients and controls using Western blotting. In a second part of the study we analyzed protein expression of GSTs in the same study cohort by ELISA. CYP1A1 expression was found to be significantly high (p<0.001) in brain tumor as compared to the normal tissues, with ~4 fold (OR=4, 95%CI=0.43-37) increase in some cases. In contrast, the expression of GSTP1 was found to be significantly low in brain tumor tissues as compared to the controls (p<0.02). This down regulation was significantly higher (OR=0.05, 95%CI=0.006-0.51; p<0.007) in certain grades of lesions. Furthermore, GSTs levels were significantly down-regulated (p<0.014) in brain tumor patients compared to controls. Statistically significant decrease in GST levels was observed in the more advanced lesions (III-IV, p<0.005) as compared to the early tissue grades (I-II). Thus, altered expression of these xenobiotic metabolizing genes may be involved in brain tumor development in Pakistani population. Investigation of expression of these genes may provide information not only for the prediction of individual cancer risk but also for the prevention of cancer.

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Section: Discussionsupporting

confidence: 88%

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Wahid¹,

Mahjabeen²,

Baig³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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“…That is why the future problem is elucidation of the networks of miRNA that regulates protein coding genes in various cells. Based on this view, we sequentially identified tumor suppressive miRNAs that regulate multiple oncogene networks in various cancer cells (10,11,15,(18)(19)(20).…”

Section: Discussionmentioning

confidence: 99%

“…The expression of miR-1 and miR-133a has been reported to be down-regulated in various cancers, and these miRNAs might have tumor suppressive functions (4,(10)(11)(12)(13). We previously reported that miR-1 and miR-133a directly regulated oncogenic LASP1 and TAGLN2 genes in human BC (14,15).…”

Section: Introductionmentioning

confidence: 93%

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Novel molecular targets regulated by tumor suppressors microRNA-1 and microRNA-133a in bladder cancer

et al. 2012

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Abstract. Our expression signatures of human cancer including bladder cancer (BC) revealed that the expression of microRNA-1 (miR-1) and microRNA-133a (miR-133a) is significantly reduced in cancer cells. In the human genome, miR-1 and miR-133a are located on the same chromosomal region (miR-1-2 and miR133a-1 on 18q11.2, and miR-1-1 and miR-133a-2 on 20q13.33) called cluster. In this study, we identified the novel molecular targets commonly regulated by miR-1 and miR-133a in BC. Genome-wide molecular target search and luciferase reporter assays showed that prothymosin-α (PTMA) and purine nucleoside phosphorylase (PNP) are directly regulated by miR-1 and miR-133a. Silencing of these two genes significantly inhibited cell proliferation and invasion, and increased apoptosis in BC cells. Immunohistochemistry showed that PTMA expression levels were significantly higher in BC compared to normal bladder epitheliums. PTMA and PNP were identified as new target genes regulated by the miR-1 and miR-133a cluster in BC. These genes may function as oncogenes contributing to cell proliferation and invasion in BC. Tumor suppressive miR-1 and miR-133a-mediated novel molecular targets may provide new insights into the potential mechanisms of BC oncogenesis.

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“…Studies have found that miR-133a regulates oncogenic transcripts in human cells, including FSCN1, EGFR, LASP1, GSTP1 and TAGLN2 (34,37,38). Therefore, upregulating miR-133a or providing exogenous analogous pharmaceutical compounds may provide effective cancer therapies for HCC, which resulted from the overexpression of these oncogenic transcripts.…”

Section: Mmp-9 Is a Direct Target Gene Of Mir-133a In Hccmentioning

confidence: 99%

MicroRNA-133a inhibits cell proliferation, colony formation ability, migration and invasion by targeting matrix metallopeptidase 9 in hepatocellular carcinoma

Chen

Zhao

et al. 2015

Molecular Medicine Reports

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Abstract. is downregulated in various types of human malignancy, including hepatocellular carcinoma (HCC), renal cell carcinoma, esophageal squamous cell carcinoma, bladder cancer, ileal carcinoid and rhabdomyosarcoma. The aim of the present study was to examine the effects of miR-133a on HCC cell proliferation, colony formation, migration and invasion. miR-133a was transfected into the HCC HepG2 and SMMC-7721 cell lines and the expression levels of miR-133a were determined; in addition, cell viability assays, colony formation assays, cell migration assays, cell invasion assays, western blot analyses and luciferase assays were performed in the HCC cell lines. The results demonstrated that miR-133a significantly inhibited cell proliferation, colony formation, migration and invasion in HepG2 and SMMC-7721 cells. To the best of our knowledge, the present study also provided the first evidence that miR-133a directly downregulated the expression of matrix metallopeptidase 9 (MMP-9) in the HCC cells. In conclusion, the results of the present study indicated that miR-133a may have suppressed cell proliferation, colony formation, migration and invasion via the downregulation of MMP-9 in HCC cell lines. Therefore, MMP-9 may be used for the development of novel molecular markers and therapeutic approaches to inhibit hepatocellular carcinoma metastasis.

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MiR-133a induces apoptosis through direct regulation of GSTP1 in bladder cancer cell lines

Cited by 82 publications

References 36 publications

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Expression of CYP1A1 and GSTP1 in Human Brain Tumor Tissues in Pakistan

Novel molecular targets regulated by tumor suppressors microRNA-1 and microRNA-133a in bladder cancer

MicroRNA-133a inhibits cell proliferation, colony formation ability, migration and invasion by targeting matrix metallopeptidase 9 in hepatocellular carcinoma

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