scholarly journals Implications of microRNA dysregulation in the development of prostate cancer

Reproduction ◽  
2017 ◽  
Vol 154 (4) ◽  
pp. R81-R97 ◽  
Author(s):  
Cintia Massillo ◽  
Guillermo N Dalton ◽  
Paula L Farré ◽  
Paola De Luca ◽  
Adriana De Siervi

MicroRNAs (miRNAs) are non-coding small RNAs that target mRNA to reduce protein expression. They play fundamental roles in several diseases, including prostate cancer (PCa). A single miRNA can target hundreds of mRNAs and coordinately regulate them, which implicates them in nearly every biological pathway. Hence, miRNAs modulate proliferation, cell cycle, apoptosis, adhesion, migration, invasion and metastasis, most of them constituting crucial hallmarks of cancer. Due to these properties, miRNAs emerged as promising tools for diagnostic, prognosis and management of cancer patients. Moreover, they come out as potential targets for cancer treatment, and several efforts are being made to progress in the field of miRNA-based cancer therapy. In this review, we will summarize the recent information about miRNAs in PCa. We will recapitulate all the miRNAs involved in the androgen pathway and the biology of PCa, focusing in PCa initiation and progression. In particular, we will describe the miRNAs associated with cell proliferation, cell cycle and apoptosis in PCa, as well as invasion, adhesion and metastatic miRNAs. We will revise the recent progress made understanding the role of circulating miRNAs identified in PCa that might be useful for PCa patient stratification. Another key aspect to be discussed in this review is miRNAs’ role in PCa therapy, including the miRNAs delivery.

Author(s):  
Shamim Mushtaq

Uninhibited proliferation and abnormal cell cycle regulation are the hallmarks of cancer. The main role of cyclin dependent kinases is to regulate the cell cycle and cell proliferation. These protein kinases are frequently down regulated or up regulated in various cancers. Two CDK family members, CDK 11 and 12, have contradicting views about their roles in different cancers. For example, one study suggests that the CDK 11 isoforms, p58, inhibits growth of breast cancer whereas, the CDK 11 isoform, p110, is highly expressed in breast tumor. Studies regarding CDK 12 show variation of opinion towards different parts of the body, however there is a consensus that upregulation of cdk12 increases the risk of breast cancer. Hence, CDK 11 and CDK 12 need to be analyzed to confirm their mechanism and their role regarding therapeutics, prognostic value, and ethnicity in cancer. This article gives an outline on both CDKs of information known up to date from Medline, PubMed, Google Scholar and Web of Science search engines, which were explored and thirty relevant researches were finalized.


2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaoyang Zhang ◽  
Cheng Wei ◽  
Hao Liang ◽  
Lei Han

Polo-like kinases (Plks) are critical regulatory molecules during the cell cycle process. This family has five members: Plk1, 2, 3, 4, and 5. Plk4 has been identified as a master regulator of centriole replication, and its aberrant expression is closely associated with cancer development. In this review, we depict the DNA, mRNA, and protein structure of Plk4, and the regulation of Plk4 at a molecular level. Then we list the downstream targets of Plk4 and the hallmarks of cancer associated with these targets. The role of Plk4 in different cancers is also summarized. Finally, we review the inhibitors that target Plk4 in the hope of discovering effective anticancer drugs. From authors’ perspective, Plk4 might represent a valuable tumor biomarker and critical target for cancer diagnosis and therapy.


2014 ◽  
Vol 912-914 ◽  
pp. 1915-1918
Author(s):  
Qing Fang ◽  
Fang Fang ◽  
Yu Lian Liu ◽  
Wen Ping Li ◽  
Li Guo Wang

CD147 is expressed on the cell surface of most tumor cells, which results in cancer cells proliferation, invasion, metastasis and angiogenes. Our previous study indicated that CD147 could promote invasion andmetastasis of prostate cancer. However the role of CD147 on cell proliferation has not to be explored inprostate cancer. In this study, the effects of CD147 on cell proliferation of hormone-independent prostatecancer (LNCaP-AI) was investigated. In the present study, cell cycle distribution was investigated by flowcytometry and cell cycle protein were analysis by wester blot. The results demonstrated that knock-donwn CD147 expression induced G0/G1 phase arrest, and expression of cyclin D1 has potential suppressed with western blot analysis. The results suggest that CD147 could inhibit cell prolifearion and as potential therapeutic application in treatment of proste cancer.


Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 10-17 ◽  
Author(s):  
Sarah E. Blutt ◽  
Timothy J. McDonnell ◽  
Tara C. Polek ◽  
Nancy L. Weigel

Abstract While the role of vitamin D in bone and mineral metabolism has been investigated extensively, the role of the vitamin D receptor in other tissues is less well understood. 1,25-dihydroxyvitamin D3 (calcitriol) can act as a differentiating agent in normal tissues and can inhibit the growth of many cancer cell lines including LNCaP prostate cancer cells. We have shown previously that calcitriol causes LNCaP cell accumulation in the G0/G1 phase of the cell cycle. In this study, we demonstrate that calcitriol also induces apoptosis of LNCaP cells. The calcitriol-induced apoptosis is accompanied by a down-regulation of Bcl-2 and Bcl-XL proteins, both of which protect cells from undergoing apoptosis. Other proteins important in apoptotic control, Bax, Mcl-1, and Bcl-Xs, are unaffected by calcitriol treatment. We find that overexpression of Bcl-2 blocks calcitriol-induced apoptosis and reduces, but does not eliminate, calcitriol-induced growth inhibition. We conclude that both regulation of cell cycle and the apoptotic pathway are involved in calcitriol action in prostate cancer cells.


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