VEGF-activated miR-144 regulates autophagic survival of prostate cancer cells against Cisplatin

Liu, Feng; Wang, Jihong; Fu, Qiang; Zhang, Xinru; Wang, Ying; Liu, Jialin; Huang, Jianwen; Lv, Xiangguo

doi:10.1007/s13277-015-4383-1

Cited by 22 publications

(20 citation statements)

References 50 publications

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“…Although the tumor suppressive effects of miR‐124 and miR‐144 were reported in previous studies , whether their expression was altered in hypoxia has not been reported yet. In this study, we observed that miR‐124 and miR‐144 were significantly downregulated in hypoxia, which might be a result of impaired Dicer expression.…”

Section: Discussionmentioning

confidence: 89%

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Hypoxia‐responsive miR‐124 and miR‐144 reduce hypoxia‐induced autophagy and enhance radiosensitivity of prostate cancer cells via suppressing PIM1

Liu

Ding

et al. 2016

Cancer Medicine

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Cancer cells in hypoxia usually make adaptive changes in cellular metabolism, such as altered autophagy. This might be a cause of enhanced radioresistance in some types of cancer. In this study, we investigated hypoxia‐responsive miRNAs in two prostate cancer cell lines (DU145 and PC3). This study firstly reported that hypoxia induces further downregulation of miR‐124 and miR‐144, which might be a result of impaired dicer expression. These two miRNAs can simultaneously target 3′UTR of PIM1. Functional study showed that miR‐124 or miR‐144 overexpression can inhibit hypoxia‐induced autophagy and enhance radiosensitivity at least via downregulating PIM1. Therefore, hypoxia induced miR‐124 and miR‐144 downregulation may contribute to a prosurvival mechanism of prostate cancer cells to hypoxia and irradiation at least through attenuated suppressing of PIM1. This finding presents a potential therapeutic target for prostate cancer.

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Section: Discussionmentioning

confidence: 89%

“…A and B). MiR‐124 and miR‐144 are two tumor suppressors of prostate cancer . The microarray analysis showed these two miRNAs were decreased dramatically in hypoxia in both DU145 and PC3 cells (Fig.…”

Section: Resultsmentioning

confidence: 96%

Hypoxia‐responsive miR‐124 and miR‐144 reduce hypoxia‐induced autophagy and enhance radiosensitivity of prostate cancer cells via suppressing PIM1

Liu

Ding

et al. 2016

Cancer Medicine

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“…Another study confirmed that the expression levels of sputum and serum miR-144-3p were significantly upregulated in the tuberculosis patients, but were found to decrease significantly after anti-tuberculosis treatment [26]. In addition, it has been reported that cisplatin-induced VEGF can suppress the expression levels of miR-144 in prostate cancer cells, which subsequently upregulates Beclin-1 to increase autophagic cell survival against cisplatin-induced cell death [27]. Chen S et al have shown that miR-144 increased autophagy in lung cancer cells by targeting TIGAR [28].…”

Section: Introductionmentioning

confidence: 92%

MicroRNA-144-3p inhibits autophagy activation and enhances Bacillus Calmette-Guérin infection by targeting ATG4a in RAW264.7 macrophage cells

et al. 2017

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MicroRNAs (miRNAs) are small noncoding nucleotides that play major roles in the response of host immune cells. Autophagy plays a key role in activating the antimicrobial host defense against Mycobacterium tuberculosis (M. tuberculosis). Whether miRNAs specifically influence the activation of macrophage autophagy during M. tuberculosis infection is largely unknown. In the present study, we demonstrate that Mycobacterium bovis Bacillus Calmette-Guérin (BCG) infection of macrophages leads to increased expression of miR-144-3p, which targets autophagy-related gene 4a (ATG4a), to inhibit autophagy activation and antimicrobial responses to BCG. Overexpression of miR-144-3p significantly decreased both mRNA and protein levels of ATG4a, inhibited the formation of autophagosomes in RAW264.7 cells and increased intracellular survival of BCG. However, transfection with miR-144-3p inhibitor led to an increase in ATG4a levels, accelerated the autophagic response in macrophages, and decreased BCG survival in macrophages. The experimental results of this study reveal a novel role of miR-144-3p in inhibiting autophagy activation by targeting ATG4a and enhancing BCG infection, and provide potential targets for developing improved treatment.

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“…In terms of chemoresistance, miR-144 reversed 5-FU and imatinib resistance respectively in HCC (461) and leukemia (462). In addition, miR-144 might promote cisplatin sensitivity in prostate cancer (463) and in thyroid carcinoma (464). Whereas miR-144-3p contributed to sunitinib resistance in RCC by targeting ARID1A, a cancer gene involved in chromatin remodeling (465).…”

Section: Drugs/non-coding Rnas Subnetworkmentioning

confidence: 99%

The Network of Non-coding RNAs in Cancer Drug Resistance

et al. 2018

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Non-coding RNAs (ncRNAs) have been implicated in most cellular functions. The disruption of their function through somatic mutations, genomic imprinting, transcriptional and post-transcriptional regulation, plays an ever-increasing role in cancer development. ncRNAs, including notorious microRNAs, have been thus proposed to function as tumor suppressors or oncogenes, often in a context-dependent fashion. In parallel, ncRNAs with altered expression in cancer have been reported to exert a key role in determining drug sensitivity or restoring drug responsiveness in resistant cells. Acquisition of resistance to anti-cancer drugs is a major hindrance to effective chemotherapy and is one of the most important causes of relapse and mortality in cancer patients. For these reasons, non-coding RNAs have become recent focuses as prognostic agents and modifiers of chemo-sensitivity. This review starts with a brief outline of the role of most studied non-coding RNAs in cancer and then highlights the modulation of cancer drug resistance via known ncRNAs based mechanisms. We identified from literature 388 ncRNA-drugs interactions and analyzed them using an unsupervised approach. Essentially, we performed a network analysis of the non-coding RNAs with direct relations with cancer drugs. Within such a machine-learning framework we detected the most representative ncRNAs-drug associations and groups. We finally discussed the higher integration of the drug-ncRNA clusters with the goal of disentangling effectors from downstream effects and further clarify the involvement of ncRNAs in the cellular mechanisms underlying resistance to cancer treatments.

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VEGF-activated miR-144 regulates autophagic survival of prostate cancer cells against Cisplatin

Cited by 22 publications

References 50 publications

Hypoxia‐responsive miR‐124 and miR‐144 reduce hypoxia‐induced autophagy and enhance radiosensitivity of prostate cancer cells via suppressing PIM1

Hypoxia‐responsive miR‐124 and miR‐144 reduce hypoxia‐induced autophagy and enhance radiosensitivity of prostate cancer cells via suppressing PIM1

MicroRNA-144-3p inhibits autophagy activation and enhances Bacillus Calmette-Guérin infection by targeting ATG4a in RAW264.7 macrophage cells

The Network of Non-coding RNAs in Cancer Drug Resistance

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