MicroRNA-21 directly targets MARCKS and promotes apoptosis resistance and invasion in prostate cancer cells

Li, Tao; Li, Dong; Sha, Jianjun; Sun, Peng; Huang, Yiran

doi:10.1016/j.bbrc.2009.03.077

Cited by 328 publications

(226 citation statements)

References 28 publications

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“…Constitutively phosphorylated MARCKS in PC3 cells could contribute to the increased motility and invasiveness shown by this line compared with LNCaP cells [31]. A previous study suggested that MARCKS partly mediated the positive effect of miR-21 on AIPC cell invasion [32]. It is the first time we have reported the proteins being regulated by miR-200b in AIPC.…”

Section: Discussionmentioning

confidence: 63%

Label free quantitative proteomics reveals the role of miR-200b in androgen-independent prostate cancer cells

Gou

et al. 2018

Clin Proteom

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Background: Our previous studies indicated that miR-200b inhibits the growth of androgen-independent prostate cancer (AIPC) cells. In this study, we employed quantitative proteomics techniques to unravel the role of miR-200b in AIPC. Results: Thirteen proteins were up-regulated in miR-200b mimics/mimics NC (negative miRNA control) and 14 proteins were down-regulated; 67 proteins were up-regulated in miR-200b inhibitor/inhibitor NC and 98 proteins were down-regulated. There were seven proteins which were both down-regulated by miR-200b mimics and up-regulated by miR-200b inhibitor, TM4SF1, YAP1, PPP1R2, MARCKS, RTN4, GLIPR2 and SUCLG1. Among these, TM4SF1, YAP1, PPP1R2, MARCKS, RTN4 were predicted as target genes of miR-200b by miRBase, while GLIPR2 and SUCLG1 were not. Methods Conclusion:This work identified several target genes of miR-200b by label free proteomics method, i.e., TM4SF1, YAP1, PPP1R2, MARCKS, RTN4, GLIPR2, and SUCLG1. The signaling pathways regulated by these proteins such as Hippo signaling may contribute to the phenotype resulting from miR-200b.

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Section: Discussionmentioning

confidence: 63%

Label free quantitative proteomics reveals the role of miR-200b in androgen-independent prostate cancer cells

Gou

et al. 2018

Clin Proteom

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“…Although several miRNAs have been found to function as either tumor metastasis promoters or suppressors (Asangani et al, 2008;Korpal et al, 2008;Li et al, 2009;Tsai et al, 2009), the exact role that miRNAs play in cervical cancer metastasis is only beginning to be uncovered. Here, we describe our microarraybased investigation into the metastatic-related miRNA expression profile of cervical squamous cancer.…”

Section: Discussionmentioning

confidence: 99%

Characterization of the MicroRNA Expression Profile of Cervical Squamous Cell Carcinoma Metastases

Ding¹,

Wu²,

Wang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Objectives: MicroRNAs (miRNAs) are important regulators of many physiological and pathological processes, including tumorigenesis and metastasis. In this study, we sought to determine the underlying molecular mechanisms of metastatic cervical carcinoma by performing miRNA profiling. Methods: Tissue samples were collected from ten cervical squamous cancer patients who underwent hysterectomy and pelvic lymph node (PLN) dissection in our hospital, including four PLN-positive (metastatic) cases and six PLN-negative (non-metastatic) cases. A miRNA microarray platform with 1223 probes was used to determine the miRNA expression profiles of these two tissue types and case groups. MiRNAs having at least 4-fold differential expression between PLN-positive and PLN-negative cervical cancer tissues were bioinformatically analyzed for target gene prediction. MiRNAs with tumor-associated target genes were validated by quantitative reverse transcription-polymerase chain reaction (RT-PCR). Results: Thirty-nine miRNAs were differentially expressed (>4-fold) between the PLN-positive and PLN-negative groups, of which, 22 were up-regulated and 17 were down-regulated. Sixty-nine percent of the miRNAs (27/39) had tumor-associated target genes, and the expression levels of six of those (miR-126, miR-96, miR-144, miR-657, miR-490-5p, and miR-323-3p) were confirmed by quantitative (q)RT-PCR. Conclusions: Six MiRNAs with predicted tumor-associated target genes encoding proteins that are known to be involved in cell adhesion, cytoskeletal remodeling, cell proliferation, cell migration, and apoptosis were identified. These findings suggest that a panel of miRNAs may regulate multiple and various steps of the metastasis cascade by targeting metastasis-associated genes. Since these six miRNAs are predicted to target tumor-associated genes, it is likely that they contribute to the metastatic potential of cervical cancer and may aid in prognosis or molecular therapy.

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“…Previously identified or proposed miR-21 targets include tropomyosin-1 (an inhibitor of anchorageindependent cell proliferation) (Zhu et al, 2008), PTEN (a negative regulator of two MMP genes, MMP2 and MMP9, and of FAK phosphorylation) (Meng et al, 2006), programmed cell death-4 (PDCD4) (Asangani et al, 2008;Frankel et al, 2008) and maspin (two proteins implicated in suppression of invasion and metastasis) (Zhu et al, 2008), and MARCKS (a protein kinase-C-substrate regulating cell motility) (Li et al, 2009). RECK also regulates proteases and suppresses growth, invasion and metastasis of tumor cells (Takahashi et al, 1998;Oh et al, 2001;Morioka et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

Hypoxia and RAS-signaling pathways converge on, and cooperatively downregulate, the RECK tumor-suppressor protein through microRNAs

et al. 2010

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Cancer cells show characteristic gene expression profiles. Recent studies support the potential importance of micro-RNA (miRNA) expression signatures as biomarkers and therapeutic targets. The membrane-anchored protease regulator RECK is downregulated in many cancers, and forced expression of RECK in tumor cells results in decreased malignancy in animal models. RECK is also essential for mammalian development. In this study, we found that RECK is a target of at least three groups of miRNAs (miR-15b/16, miR-21 and miR-372/373); that RECK mutants lacking the target sites for these miRNA show augmented tumor/metastasis-suppressor activities; and that miR-372/373 are upregulated in response to hypoxia through HIF1a and TWIST1, whereas miR-21 is upregulated by RAS/ERK signaling. These data indicate that the hypoxia-and RAS-signaling pathways converge on RECK through miRNAs, cooperatively downregulating this tumor suppressor and thereby promoting malignant cell behavior.

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MicroRNA-21 directly targets MARCKS and promotes apoptosis resistance and invasion in prostate cancer cells

Cited by 328 publications

References 28 publications

Label free quantitative proteomics reveals the role of miR-200b in androgen-independent prostate cancer cells

Label free quantitative proteomics reveals the role of miR-200b in androgen-independent prostate cancer cells

Characterization of the MicroRNA Expression Profile of Cervical Squamous Cell Carcinoma Metastases

Hypoxia and RAS-signaling pathways converge on, and cooperatively downregulate, the RECK tumor-suppressor protein through microRNAs

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