Potential involvement of mi-RNA 574-3p in progression of prostate cancer: A bioinformatic study

Ashraf, Naeem Mahmood; Imran, Komal; Kastner, David W.; Ikram, Khadija; Mushtaq, Ayesha; Hussain, Aadil; Zeeshan, Nadia

doi:10.1016/j.mcp.2017.07.002

Cited by 11 publications

(9 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is well characterized that aberrant expression of miRNAs is one of hallmarks of carcinogenesis 27. Recent years, many researches carried out miRNA profiling of prostate cancer tissues and discovered several miRNAs with oncogene or tumor suppressor potential 20,28,29.…”

Section: Discussionmentioning

confidence: 99%

<p>miR-129-5p inhibits prostate cancer proliferation via targeting ETV1</p>

Gao¹,

Xiu²,

Yang³

et al. 2019

OTT

View full text Add to dashboard Cite

Background Prostate cancer is one of the most commonly diagnosed diseases in males. Methods RT-qPCR was used to detect miR-129-5p expression in tumor tissues and adjacent normal tissues from patients with prostate cancer. The cell proliferation assay and colony forming assay were used to study the role of miR-129-5p in mediating prostate cancer cell growth. Bioinformatic analysis and dual luciferase assay were performed to predict and confirm ETV1 as a target gene of miR-129-5p. Results We found that miR-129-5p levels were decreased significantly in human prostate cancer tissues compared with matched normal tissues from patients with prostate cancer. Overexpression of miR-129-5p suppressed prostate cancer cell growth while antagonist of miR-129-5p promoted cell proliferation in immortal prostate cell line RWPE-1. In addition, elevation of miR-129-5p decreased ETV1 expression in prostate cancer cells while downregulation of miR-129-5p increased ETV1 expression in RWPE-1. Mechanistically, ETV1 is confirmed a direct target of miR-129-5p in prostate cancer cells. Through repression of ETV1 expression, miR-129-5p could inactivate YAP signaling in prostate cancer cells. In addition, overexpression of ETV1 attenuated miR-129-5p induced cell proliferation in prostate cancer cells. Correlation analysis further revealed that there was a negative correlation between miR-129-5p levels and ETV1 mRNA levels in tumor tissues from patients with prostate cancer. Conclusion Our results identified miR-129-5p as a tumor suppressor in prostate cancer via repression of ETV1.

show abstract

Section: Discussionmentioning

confidence: 99%

<p>miR-129-5p inhibits prostate cancer proliferation via targeting ETV1</p>

Gao¹,

Xiu²,

Yang³

et al. 2019

OTT

View full text Add to dashboard Cite

show abstract

“…The competitive regulatory network formed between LncRNA and mRNA plays an critical regulatory role in the metastasis and apoptosis of glioma [18]. MicroRNA (mi RNA) are key nodes in the network that regulate the life function of signaling in cells [19,20]. Mi RNA-mediated posttranscriptional regulation is involved in the regulation of many cell life processes such as cell cycle progression, differentiation and stress response [21,22].…”

Section: Introductionmentioning

confidence: 99%

Knockdown of long non-coding RNA LINC00467 inhibits glioma cell progression via modulation of E2F3 targeted by miR-200a

Gao

Duan

et al. 2020

Cell Cycle

View full text Add to dashboard Cite

Studies have found that LINC00467 is an important regulator of cancer. However, the function of LINC00467 in glioma cell is unclear. Therefore, this experimental design based on LINC00467 to explore its mechanism of action in glioma cell. RT-qPCR was used to detect the expression of LINC0046 and miR-200a in glioma cell lines. MTT assay, Edru assay and Transwell assay and flow cytometry were used to detect the effects of LINC0046 and miR-200a on PC cell proliferation, migration and apoptosis. Target gene prediction and screening, luciferase reporter assays were used to validate downstream target genes for LINC0046 and miR-200a. Western blotting was used to detect the protein expression of E2F3. The tumor changes in mice were detected by in vivo experiments in nude mice. LINC00467 was up-regulated in glioma cells. Knockdown of LINC00467 inhibited the viability, migration and invasion of glioma cells. In glioma cells, miR-200a was significantly reduced, while E2F3 was significantly rised. LINC00467 negatively regulated the expression of miR-200a in gliomas, while miR-200a negatively regulated the expression of E2F3 in gliomas. INC00467 promoted the development of glioma by inhibiting miR-200a and promoting E2F3 expression. LINC00467 may be a potential therapeutic target for gliomas. ARTICLE HISTORY

show abstract

“…We further dissected the mechanisms of how MSCs promote the stemness of PCa MSCs cells by focusing on the Jagged1-Notch1 signaling pathway. One study showed that Notch was a positive regulator of PCa stemness [ 30 ]. Our results showed that MSCs promoted Notch signaling-related gene expression in PCa MSCs cells.…”

Section: Resultsmentioning

confidence: 99%

Bone marrow mesenchymal stem cells promote prostate cancer cell stemness via cell–cell contact to activate the Jagged1/Notch1 pathway

Cheng

Duan

et al. 2021

Cell Biosci

View full text Add to dashboard Cite

Background Mesenchymal stem cells (MSCs) play a crucial role in cancer development and tumor resistance to therapy in prostate cancer, but the influence of MSCs on the stemness potential of PCa cells by cell–cell contact remains unclear. In this study, we investigated the effect of direct contact of PCa cells with MSCs on the stemness of PCa and its mechanisms. Methods First, the flow cytometry, colony formation, and sphere formation were performed to determine the stemness of PCaMSCs, and the expression of stemness-related molecules (Sox2, Oct4, and Nanog) was investigated by western blot analysis. Then, we used western blot and qPCR to determine the activity levels of two candidate pathways and their downstream stemness-associated pathway. Finally, we verified the role of the significantly changed pathway by assessing the key factors in this pathway via in vitro and in vivo experiments. Results We established that MSCs promoted the stemness of PCa cells by cell–cell contact. We here established that the enhanced stemness of PCaMSCs was independent of the CCL5/CCR5 pathway. We also found that PCaMSCs up-regulated the expression of Notch signaling-related genes, and inhibition of Jagged1-Notch1 signaling in PCaMSCs cells significantly inhibited MSCs-induced stemness and tumorigenesis in vitro and in vivo. Conclusions Our results reveal a novel interaction between MSCs and PCa cells in promoting tumorigenesis through activation of the Jagged1/Notch1 pathway, providing a new therapeutic target for the treatment of PCa.

show abstract

Potential involvement of mi-RNA 574-3p in progression of prostate cancer: A bioinformatic study

Cited by 11 publications

References 50 publications

<p>miR-129-5p inhibits prostate cancer proliferation via targeting ETV1</p>

<p>miR-129-5p inhibits prostate cancer proliferation via targeting ETV1</p>

Knockdown of long non-coding RNA LINC00467 inhibits glioma cell progression via modulation of E2F3 targeted by miR-200a

Bone marrow mesenchymal stem cells promote prostate cancer cell stemness via cell–cell contact to activate the Jagged1/Notch1 pathway

Contact Info

Product

Resources

About