MicroRNA-21 promotes cell proliferation and down-regulates the expression of programmed cell death 4 (PDCD4) in HeLa cervical carcinoma cells

Yao, Qing; Xu, Hui; Zhang, Qianqian; Zhou, Hui; Qu, Liang‐Hu

doi:10.1016/j.bbrc.2009.08.044

Cited by 183 publications

(142 citation statements)

References 23 publications

Supporting

Mentioning

132

Contrasting

Unclassified

Order By: Relevance

“…Specifically, miR-21 has been found to be overexpressed in numerous different solid tumors. Altered miR-21 has been found to be associated with the proliferation, invasion and apoptosis of malignant cells by targeting and downregulating a number of tumor suppressors, including PTEN (6,7), programmed cell death 4 (PDCD4) (8)(9)(10)(11), bcl-2 and tropomyosin l (TPM1) (12)(13), bone morphogenetic protein receptor II (BMPRII) (14) and sprouty 2 (SPRY2) (15). These findings imply that miR-21 plays a fundamental role in malignant behavior and transformation.…”

Section: Introductionmentioning

confidence: 99%

microRNA-21 overexpression contributes to cell proliferation by targeting PTEN in endometrioid endometrial cancer

et al. 2012

View full text Add to dashboard Cite

Abstract. The aim of this study was to investigate the role of microRNA-21 (miR-21) in the regulation of phosphatase and tensin homolog deleted from chromosome-10 (PTEN) expression and proliferation of endometrioid endometrial cancer (EEC) cells. We performed a qRT-PCR assay with miR-21 and PTEN in 16 paired EEC tumor tissues and adjacent non-tumor endometrium. To investigate the regulation of PTEN by miR-21, we designed gain-and loss-of-function of miR-21 experiments in the KLE cell line by transfection with a synthetic miR-21 mimic and inhibitor. To validate the putative binding site of miR-21 in the 3' untranslated region (3'-UTR) of PTEN messenger RNA (mRNA), a dual-luciferase reporter assay was carried out. To evaluate the potential effect of miR-21 on EEC proliferation, we performed both overexpression experiments, using an miR-21 mimic, and inhibition assays, using an miR-21 inhibitor. miR-21 was overexpressed in EEC and was inversely correlated with PTEN protein expression (P<0.001). miR-21 regulated PTEN protein expression and cell proliferation in the KLE cell line and the direct binding of miR-21 to the PTEN 3'-UTR was confirmed using a dual-luciferase reporter assay. The upregulation of miR-21 led to a significant decrease in the PTEN protein expression level (P=0.007). The downregulation of miR-21 led to a significant increase in PTEN protein (P=0.002). The expression of luciferase in the wt-PTEN-3'-UTR-pGL3 group was downregulated in the presence of the miR-21 mimic (P=0.001). miR-21 was overexpressed in EEC. In conclusion, we demonstrated that the expression of PTEN protein, but not mRNA, was negatively directly regulated by miR-21 in the KLE cell line. The overexpression of miR-21 modulated EEC cell proliferation through the downregulation of PTEN.

show abstract

Section: Introductionmentioning

confidence: 99%

microRNA-21 overexpression contributes to cell proliferation by targeting PTEN in endometrioid endometrial cancer

et al. 2012

View full text Add to dashboard Cite

show abstract

“…Previous reports from other labs and our lab have shown that many miRNAs are aberrantly expressed in cervical cancer and that miRNAs can act as tumor suppressors (e.g., miR-302-367, miR-424, miR-214) [9][10][11][12] or enhancers (e.g., miR-205, miR-21, miR-19a/b) [13][14][15]. Although some progress has been achieved in the past decades, much more effort is needed to elucidate the occurrence and mechanism of cervical cancer.…”

Section: Introductionmentioning

confidence: 62%

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

et al. 2013

View full text Add to dashboard Cite

Edited by Tamas DalmayKeywords: microRNA microRNA-7 X-linked inhibitor of apoptosis protein Cell apoptosis Cervical cancer a b s t r a c t Our study demonstrated the functions of microRNA-7 (miR-7) in cervical cancer. The overexpression of miR-7 in the cervical cancer cell lines HeLa and C-33A suppressed cell viability and promoted cell apoptosis, whereas the inhibition of miR-7 had opposite effects. Furthermore, an oncogene, Xlinked inhibitor of apoptosis protein (XIAP), was identified as a new target of miR-7, and the ectopic expression of XIAP rescued the effects induced by miR-7 in HeLa and C-33A cells. These results indicate that miR-7 targeted and downregulated the oncogene XIAP to regulate the effect of miR-7 on apoptosis and malignant behaviors of HeLa and C-33A cells.

show abstract

“…This result was confirmed by reduction of PDCD4, a direct target of miR-21 in the HCK1T cells expressing E6D25E or E6Pro ( Figure 3F). The functions of PDCD4 involve apoptosis, blocking of translation and inhibition of tumor growth (Yao et al, 2009). Previous reports showed that high expression of miR-21 leads to decreased PDCD4 expression, increased expression of interleukin (IL)-10 and decreased NFκB activity (Sheedy et al, 2010).…”

Section: And Expression Of Human Immune Response Genesmentioning

confidence: 99%

Activities of E6 Protein of Human Papillomavirus 16 Asian Variant on miR-21 Up-regulation and Expression of Human Immune Response Genes

Chopjitt

Pientong²,

Bumrungthai³

et al. 2015

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

MicroRNA-21 promotes cell proliferation and down-regulates the expression of programmed cell death 4 (PDCD4) in HeLa cervical carcinoma cells

Cited by 183 publications

References 23 publications

microRNA-21 overexpression contributes to cell proliferation by targeting PTEN in endometrioid endometrial cancer

microRNA-21 overexpression contributes to cell proliferation by targeting PTEN in endometrioid endometrial cancer

MicroRNA‐7 downregulates XIAP expression to suppress cell growth and promote apoptosis in cervical cancer cells

Activities of E6 Protein of Human Papillomavirus 16 Asian Variant on miR-21 Up-regulation and Expression of Human Immune Response Genes

Contact Info

Product

Resources

About