miR-1825 Accelerates Cell Proliferation and Inhibits Cell Apoptosis of Prostate Cancer via Targeting Suppressor of Cancer Cell Invasion

Prostate cancer (PC) is one major carcinoma threat to the health of males. microRNAs (miRNAs) are short non-coding transcripts with about 23 nt in length. Booming evidence has verified the various roles of miRNAs in human tumors. miR-1825 was once demonstrated to be highly expressed in PC, but the potential role of miR-1825 in PC has never been clarified yet. This work aimed to explore the function of miR-1825 and reveal the underlying modulation mechanism in PC. First, miR-1825 was detected to be elevated in PC cells compared with normal prostate cells, as proved by RT-qPCR. After miR-1825 expression was inhibited, cell proliferation was hindered and cell apoptosis was promoted, which was observed by CCK8, colony formation, TUNEL staining and western blot assays. Bioinformatics tools discovered the targeting of suppressor of cancer cell invasion (SCAI) by miR-1825, which was further confirmed by luciferase reporter assay. Then the suppression of miR-1825 on SCAI protein expression was verified by western blotting. Eventually, rescue assays were implemented and affirmed the miR-1825/SCAI axis in PC cells. In conclusion, our present research disclosed the oncogenic role of miR-1825 and the miR-1825/SCAI pathway in PC. These findings gave new clues for the therapy of PC.

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Inhibition of cancer cell-derived exosomal microRNA-183 suppresses cell growth and metastasis in prostate cancer by upregulating TPM1

Cancer Cell International ◽

10.1186/s12935-020-01686-x ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Yanping Dai ◽

Xiaoqin Gao

Keyword(s):

Prostate Cancer ◽

Cell Proliferation ◽

Cancer Cell ◽

Prostate Cancer Cell ◽

Expression Patterns ◽

Luciferase Reporter ◽

Migration And Invasion ◽

Invasion And Migration ◽

And Migration

Abstract Background Emerging evidence continues to highlight the significant role of microRNAs (miRNAs) in the regulation of cancer growth and metastasis. Herein, the current study aimed to elucidate the role of exosomal miR-183 in prostate cancer development. Methods Initially, public microarray-based gene expression profiling of prostate cancer was employed to identify differentially expressed miRNAs. The putative target gene TPM1 of miR-183 was subsequently predicted, followed by the application of a luciferase reporter assay and examination of the expression patterns in prostate cancer patients and cell lines. The effects of miR-183 and TPM1 on processes such as cell proliferation, invasion and migration were evaluated using in vitro gain- and loss-of-function experiments. The effect of PC3 cells-derived exosomal miR-183 was validated in LNCaP cells. In vivo experiments were also performed to examine the effect of miR-183 on prostate tumor growth. Results High expression of miR-183 accompanied with low expression of TPM1 was detected in prostate cancer. Our data indicated that miR-183 could target and downregulate TPM1, with the overexpression of miR-183 and exosomal miR-183 found to promote cell proliferation, migration, and invasion in prostate cancer. Furthermore, the tumor-promoting effect of exosome-mediated delivery of miR-183 was subsequently confirmed in a tumor xenograft model. Conclusions Taken together, the key findings of our study demonstrate that prostate cancer cell-derived exosomal miR-183 enhance prostate cancer cell proliferation, invasion and migration via the downregulation of TPM1, highlighting a promising therapeutic target against prostate cancer.

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Role of monocyte-lineage cells in prostate cancer cell invasion and tissue factor expression

The Prostate ◽

10.1002/pros.21202 ◽

2010 ◽

Vol 70 (15) ◽

pp. 1672-1682 ◽

Cited By ~ 17

Author(s):

Paul F. Lindholm ◽

Yi Lu ◽

Brian P. Adley ◽

Tudor Vladislav ◽

Borko Jovanovic ◽

...

Keyword(s):

Prostate Cancer ◽

Tissue Factor ◽

Cancer Cell ◽

Cell Invasion ◽

Prostate Cancer Cell ◽

Tissue Factor Expression ◽

Cancer Cell Invasion ◽

Factor Expression

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Abstract 4335: The role of fibroblasts in prostate cancer cell invasion in tumor microenvironments

10.1158/1538-7445.am2017-4335 ◽

2017 ◽

Author(s):

Tariq Shah ◽

Flonne Wildes ◽

Dmitri Artemov ◽

Zaver M. Bhujwalla

Keyword(s):

Prostate Cancer ◽

Cancer Cell ◽

Cell Invasion ◽

Prostate Cancer Cell ◽

Cancer Cell Invasion ◽

Tumor Microenvironments

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Periprostatic Adipose Tissue Favors Prostate Cancer Cell Invasion in an Obesity-Dependent Manner: Role of Oxidative Stress

Molecular Cancer Research ◽

10.1158/1541-7786.mcr-18-0748 ◽

2019 ◽

Vol 17 (3) ◽

pp. 821-835 ◽

Cited By ~ 21

Author(s):

Victor Laurent ◽

Aurélie Toulet ◽

Camille Attané ◽

Delphine Milhas ◽

Stéphanie Dauvillier ◽

...

Keyword(s):

Oxidative Stress ◽

Prostate Cancer ◽

Adipose Tissue ◽

Cancer Cell ◽

Cell Invasion ◽

Prostate Cancer Cell ◽

Dependent Manner ◽

Cancer Cell Invasion

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EB1 Restricts Breast Cancer Cell Invadopodia Formation and Matrix Proteolysis via FAK

Cells ◽

10.3390/cells10020388 ◽

2021 ◽

Vol 10 (2) ◽

pp. 388

Author(s):

Brice Chanez ◽

Kevin Ostacolo ◽

Ali Badache ◽

Sylvie Thuault

Keyword(s):

Breast Cancer ◽

Cancer Cell ◽

Cell Invasion ◽

Focal Adhesions ◽

Matrix Degradation ◽

Cancer Cell Invasion ◽

Wild Type ◽

Spatial Regulation ◽

Invadopodia Formation

Regulation of microtubule dynamics by plus-end tracking proteins (+TIPs) plays an essential role in cancer cell migration. However, the role of +TIPs in cancer cell invasion has been poorly addressed. Invadopodia, actin-rich protrusions specialized in extracellular matrix degradation, are essential for cancer cell invasion and metastasis, the leading cause of death in breast cancer. We, therefore, investigated the role of the End Binding protein, EB1, a major hub of the +TIP network, in invadopodia functions. EB1 silencing increased matrix degradation by breast cancer cells. This was recapitulated by depletion of two additional +TIPs and EB1 partners, APC and ACF7, but not by the knockdown of other +TIPs, such as CLASP1/2 or CLIP170. The knockdown of Focal Adhesion Kinase (FAK) was previously proposed to similarly promote invadopodia formation as a consequence of a switch of the Src kinase from focal adhesions to invadopodia. Interestingly, EB1-, APC-, or ACF7-depleted cells had decreased expression/activation of FAK. Remarkably, overexpression of wild type FAK, but not of FAK mutated to prevent Src recruitment, prevented the increased degradative activity induced by EB1 depletion. Overall, we propose that EB1 restricts invadopodia formation through the control of FAK and, consequently, the spatial regulation of Src activity.

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