Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells

He, Jin-Hua; Zhang, Jingzhi; Han, Zeping; Wang, Li; Lv, Yu; Li, Yuguang

doi:10.1186/preaccept-1983004361129219

Cited by 28 publications

(38 citation statements)

References 35 publications

(38 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although radiotherapy chemotherapy and primary treatment approaches for CRC can prolong life expectancy and reduce patient burden, the CRC prognosis remains poor (22,23). LncRNAs were recently demonstrated to play vital roles as major regulators of gene expression and cancer cell proliferation (24) in multiple cancers. Several lncRNAs have been identified as regulators in CRC cell proliferation and metastasis (25).…”

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Chen

et al. 2019

Front. Oncol.

View full text Add to dashboard Cite

This study aimed to identify the roles of the long non-coding RNA LINC00114 in colorectal cancer (CRC) development. The expression levels of LINC00114 and miR-133b in CRC were determined by reverse transcription (RT)-polymerase chain reaction (PCR) and the functions of LINC00114 in CRC were evaluated in vitro and in vivo. Methylationspecific PCR assay was performed to detect the miR-133b promoter methylation in CRC cells. Bioinformatics analysis, RNA immunoprecipitation, dual luciferase assay, RNA pull-down, co-immunoprecipitation (IP), and chromatin IP (ChIP) assays were used to elucidate whether LINC00114 could recruit EZH2/DNMT1 and bind to the miR-133b promoter region, leading to dysregulated methylation and the depression of miR-133b. The expression levels of DNA methyltransferases (DNMTs), EZH2, and nucleoporin 214(NUP214) were analyzed by western blotting. Data showed that LINC00114 was highly expressed, whereas miR-133b was downregulated in the CRC tissues and cells. In vitro, silencing LINC00114 inhibited cell proliferation and impeded cell cycle at the G1/S phase by upregulating miR-133b. In vivo, LINC00114 knockdown reduced tumor growth. Further analysis showed that the methylation in miR-133b promoter region was increased in the CRC and silencing LINC00114 increased miR-133b expression through depressing methylation of its promoter region. ChIP-PCR experiments demonstrated that EZH2 and DNMT1 could bind to the miR-133b promoter region and it was abolished by LINC00114 knockdown. sh-EZH2 reversed the overexpression of DNMTs and CRC cell cycle progression induced by the LINC00114 upregulation. LINC00114 could regulate the NUP214 protein expression by sponging miR-133b. These results demonstrated that LINC00114 suppressed miR-133b expression via EZH2/DNMT1-mediated methylation of its promoter region, indicating that LINC00114 might be a potential novel target for CRC diagnosis and treatment.

show abstract

Section: Discussionmentioning

confidence: 99%

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Chen

et al. 2019

Front. Oncol.

View full text Add to dashboard Cite

show abstract

“…Increased expression of PCGEM1 gene is related to increased cell proliferation and colony formation, an indication that the altered expression of this gene contribute to the development and/or progression of prostate cancer in androgen independent cells [23]. Furthermore, the use of an siRNA PCGEM1 by He et al [80] inhibited cell growth and reduced cell migration and colony formation in LNCaP cells, confirming that the key role of this gene in prostate cancer associated to hyperproliferation and (or) metastasis [23]. Yet, PCGEM1 gene is also overexpressed in castration resistance prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

γ‐oryzanol reduces caveolin‐1 and PCGEM1 expression, markers of aggressiveness in prostate cancer cell lines

et al. 2015

View full text Add to dashboard Cite

show abstract

“…More interestingly, the roles of miRNA have proven to be indispensable in affecting cancer biology, including proliferation, autophagy, apoptosis, and invasiveness [ 10 - 14 ]. Accumulating data have suggested that miRNAs are involved in the tumorigenesis and progression of prostate cancer and act as a tumor suppressors or oncogenes [ 15 - 20 ]. MiR-203, a putative tumor suppressor gene, has been shown to inhibit cell proliferation and invasion and modulate the chemotherapy response in a variety of tumor cells, including lung cancer cells, glioma cells, and breast cancer cells [ 21 - 24 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-203 down-regulates Rap1A and suppresses cell proliferation, adhesion and invasion in prostate cancer

Xiang

Bian

Wang

et al. 2015

J Exp Clin Cancer Res

View full text Add to dashboard Cite

ObjectiveEvidence supports an important role for miR-203 in the regulation of the proliferation, migration and invasion of prostate cancer (PCa) cells. However, the exact mechanisms of miR-203 in PCa are not entirely clear.MethodsWe examined the expression of miR-203 in prostate cancer tissues, adjacent normal tissues, PCa cell lines and normal prostate epithelial cells by qRT-PCR. Then, the effects of miR-203 or Rap1A on proliferation, adhesion and invasion of PCa cells were assayed using CKK-8, adhesion analysis, and transwell invasion assays. Luciferase reporter assay was performed to assess miR-203 binding to Rap1A mRNA. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice.ResultsHere, we confirmed that the expression of miR-203 was significantly downregulated in prostate cancer specimens compared with matched adjacent normal prostate specimens. Mechanistic dissection revealed that miR-203 mediated cell proliferation, adhesion and invasion in vitro, and tumor growth in vivo, as evidenced by reduced RAC1, p-PAK1, and p-MEK1 expression. In addition, we identified Rap1A as a direct target suppressed by miR-203, and there was an inverse relationship between the expression of miR-203 and Rap1A in PCa. Knockdown of Rap1A phenocopied the effects of miR-203 on PCa cell growth and invasion. Furthermore, Rap1A over-expression in PCa cells partially reversed the effects of miR-203-expression on cell adhesion and invasion.ConclusionsThese findings provide further evidence that a crucial role for miR-203 in inhibiting metastasis of PCa through the suppression of Rap1A expression.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-015-0125-x) contains supplementary material, which is available to authorized users.

show abstract

Reciprocal regulation of PCGEM1 and miR-145 promote proliferation of LNCaP prostate cancer cells

Cited by 28 publications

References 35 publications

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

Long Non-coding RNA LINC00114 Facilitates Colorectal Cancer Development Through EZH2/DNMT1-Induced miR-133b Suppression

γ‐oryzanol reduces caveolin‐1 and PCGEM1 expression, markers of aggressiveness in prostate cancer cell lines

MiR-203 down-regulates Rap1A and suppresses cell proliferation, adhesion and invasion in prostate cancer

Contact Info

Product

Resources

About