MiR-199a suppresses prostate cancer paclitaxel resistance by targeting YES1

Chen, Lei; Cao, Hongwen; Feng, Yigeng

doi:10.1007/s00345-017-2143-0

Cited by 36 publications

(30 citation statements)

References 24 publications

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“…26,27 Downregulation of miR-199a-3p contributes to paclitaxel resistance in PCa cells. 28 In the present study, we showed that miR-199a/b-3p (the passenger strands) had potent antitumor activity and controlled three oncogenes (CHKA, CDC6 and NCAPH) in CRPC cells. Aberrant expression of NCAPH was closely associated with prognosis and stage of PCa patients.…”

Section: Chka Cdc6 Ncaphmentioning

confidence: 52%

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Micro‐ribonucleic acid expression signature of metastatic castration‐resistant prostate cancer: Regulation of NCAPH by antitumor miR‐199a/b‐3p

et al. 2019

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Objectives To identify oncogenes regulated by micro‐ribonucleic acid, miR‐199a/b‐3p, in metastatic castration‐resistant prostate cancer. Methods Advanced ribonucleic acid sequencing technologies were applied to construct a micro‐ribonucleic acid expression signature using metastatic castration‐resistant prostate cancer autopsy specimens. Ectopic expression of mature micro‐ribonucleic acids or small‐interfering ribonucleic acids were applied to functional assays for cancer cell lines. Genome‐wide gene expression and in silico database analyses were carried out to predict micro‐ribonucleic acid targets. Results Ectopic expression of miR‐199a/b inhibited cancer cell aggressiveness. The gene coding for non‐structural maintenance of chromosomes condensin I complex subunit H was directly regulated by miR‐199a/b‐3p. High expression of condensin I complex subunit H was significantly associated with poor disease‐free survival by The Cancer Genome Atlas database analysis (P < 0.0001). Overexpression of condensin I complex subunit H was detected in hormone‐sensitive prostate cancer and castration‐resistant prostate cancer specimens, and knockdown assays showed that its expression enhanced cancer cell migration and invasive abilities. Conclusions Small ribonucleic acid sequencing of metastatic castration‐resistant prostate cancer specimens showed the presence of several antitumor micro‐ribonucleic acids whose targets are involved in hormone‐sensitive prostate cancer and metastatic castration‐resistant prostate cancer pathogenesis. Condensin I complex subunit H seems to be a promising diagnostic marker and therapeutic target for this disease. Our approach, based on the roles of anti‐tumor micro‐ribonucleic acids and their targets, will contribute to an improved understanding of the molecular pathogenesis of hormone‐sensitive prostate cancer and metastatic castration‐resistant prostate cancer.

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Section: Chka Cdc6 Ncaphmentioning

confidence: 52%

“…In imatinib‐resistant chronic myeloid leukemia cells, downregulation of miR‐199a‐5p and miR‐199b‐5p was detected, and their overexpression improved drug sensitivity to imatinib . Downregulation of miR‐199a‐3p contributes to paclitaxel resistance in PCa cells …”

Section: Discussionmentioning

confidence: 99%

Micro‐ribonucleic acid expression signature of metastatic castration‐resistant prostate cancer: Regulation of NCAPH by antitumor miR‐199a/b‐3p

et al. 2019

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“…miR‐199a‐5p has been reported as a tumour suppressor by inhibiting the growth and inducing apoptosis in cancer cells . Moreover, miR‐199a‐5p also promotes chemotherapeutic‐induced apoptosis in various cancer cell types . Notably, miR‐199a‐5p inhibition improves the survival of mesenchymal stem cells .…”

Section: Discussionmentioning

confidence: 99%

Inhibition of microRNA‐199a‐5p ameliorates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 neurons by targeting Brg1 to activate Nrf2/HO‐1 signalling

Liang

Tong

et al. 2020

Clin Exp Pharma Physio

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MicroRNAs (miRNAs) have emerged as critical regulators of neuronal survival during cerebral ischaemia/reperfusion injury. Accumulating evidence has shown that miR‐199a‐5p plays a crucial role in regulating apoptosis and survival in various cell types. However, whether miR‐199a is involved in regulating neuronal survival during cerebral ischaemia/reperfusion injury remains unknown. In this study, we aimed to explore the biological role of miR‐199a‐5p in regulating neuronal injury induced by oxygen‐glucose deprivation/reoxygenation (OGD/R), an in vitro cellular model of cerebral ischaemia and reperfusion injury. We found that miR‐199a‐5p expression was significantly altered in neurons in response to OGD/R treatment. Overexpression of miR‐199a‐5p facilitated OGD/R‐induced apoptosis and reactive oxygen species (ROS) production, whereas miR‐199a‐5p inhibition alleviated OGD/R‐induced apoptosis and ROS production. Notably, our results identified Brahma‐related gene 1 (Brg1) as a target gene of miR‐199a‐5p. Moreover, inhibition of miR‐199a‐5p promoted the activation of nuclear factor‐erythroid‐2‐related factor‐2 (Nrf2)/heme oxygenase‐1 (HO‐1) signalling via targeting Brg1. However, silencing of Brg1 markedly reversed the miR‐199a‐5p inhibition‐mediated neuroprotective effect. Taken together, our results suggest that downregulation of miR‐199a‐5p protects neurons from OGD/R‐induced neuronal injury through upregulating Brg1 to activate Nrf2/HO‐1 signalling. The miR‐199a‐5p/Brg1/Nrf2/HO‐1 regulation axis may play an important role in regulating neuronal survival during cerebral ischaemic/reperfusion injury in vivo.

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“…21 More and more evidence has proved that YES1 is upregulated in several cancer types, such as thyroid, gastric, and PCa. [22][23][24] YES1, a notable member of Src family tyrosinekinases, and has been widely documented to regulate cell growth, adhesion, and F I G U R E 5 YES1 was overexpressed in PCa tissues and cells and negatively associated with the miR-140. A, qRT-PCR results showed that YES1 mRNA was significantly upregulated in PCa tissues compared to the matched adjacent nontumorous tissues.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐140 inhibit prostate cancer cell invasion and migration by targeting YES proto‐oncogene 1

Zhao

Jie

et al. 2019

J of Cellular Biochemistry

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Prostate cancer (PCa), which is an aggressive malignancy of the male genitourinary system. In the present study, the effects of microRNA‐140 (miR‐140) on PCa were determined. We transfected miR‐140 mimics or negative control into PCa cells, and we used MTT, wound healing, and Transwell assays for determining the capacities of miR‐140 in cell proliferation, migration, and invasion, respectively. We also confirmed the relationship between miR‐140 and YES proto‐oncogene 1 (YES1) using Luciferase reporter assay. The results showed that miR‐140 was downregulated in PCa cells and tissues, and overexpression of miR‐140 could significantly suppress their capacities of proliferation, migration, and invasion. Moreover, YES1 was shown to be a direct target of miR‐140. Moreover, miR‐140 expression is negatively correlated with YES1 levels. miR‐140 exhibits significant tumor‐suppressive effects in PCa by inhibiting YES1. The study indicated that miR‐140 and YES1 could be the potential targets for PCa therapy.

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MiR-199a suppresses prostate cancer paclitaxel resistance by targeting YES1

Abstract: The downregulation of miR-199a contributes to PTX resistance in prostate cancer. YES1 mediates the regulation of miR-199a in prostate cancer PTX resistance. This miR-199a replacement therapy has potential to overcome PTX resistance.

Cited by 36 publications

References 24 publications

Micro‐ribonucleic acid expression signature of metastatic castration‐resistant prostate cancer: Regulation of NCAPH by antitumor miR‐199a/b‐3p

Micro‐ribonucleic acid expression signature of metastatic castration‐resistant prostate cancer: Regulation of NCAPH by antitumor miR‐199a/b‐3p

Inhibition of microRNA‐199a‐5p ameliorates oxygen‐glucose deprivation/reoxygenation‐induced apoptosis and oxidative stress in HT22 neurons by targeting Brg1 to activate Nrf2/HO‐1 signalling

MicroRNA‐140 inhibit prostate cancer cell invasion and migration by targeting YES proto‐oncogene 1

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