GFRα2 prompts cell growth and chemoresistance through down-regulating tumor suppressor gene PTEN via Mir-17-5p in pancreatic cancer

Gu, Jiangning; Wang, Di; Zhang, Jiaqiang; Zhu, Yi; Liu, Ying; Chen, Hao; Shi, Minmin; Wang, Xuelong; Shen, Baiyong; Deng, Xiaxing; Zhan, Qimin; Wei, Gang; Peng, Chenghong

doi:10.1016/j.canlet.2016.06.016

Cited by 56 publications

(42 citation statements)

References 31 publications

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“…46 The Mir-17-5p/PTEN axis has been reported to be highly related to chemoresistance in prostate cancer and pancreatic cancer. 47, 48 Inhibition of miR-26a or miR-214 could induce more apoptosis in primary cultured CLL cells via downregulate expression of PTEN. 49 In this report, we utilized in silico algorithms to find miR-3142 target genes in the PI3K/ Akt survival pathway and found that PTEN was a potential target of miR-3142.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Functional screen analysis reveals miR-3142 as central regulator in chemoresistance and proliferation through activation of the PTEN-AKT pathway in CML

et al. 2017

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Chronic myeloid leukemia (CML) is caused by the constitutively active BCR-ABL tyrosine kinase. Although great progress has been made for improvement in clinical treatment during the past decades, it is common for patients to develop chemotherapy resistance. Therefore, further exploring novel therapeutic strategies are still crucial for improving disease outcome. MicroRNAs (miRNAs) represent a novel class of genes that function as negative regulators of gene expression. Recently, miRNAs have been implicated in several cancers. Previously, we identified 41 miRNAs that were dysregulated in resistant compared with adriamycin (ADR)-sensitive parental cells in CML. In the present study, we reported that miR-3142 are overexpressed in ADR-resistant K562/ADR cells and CML/multiple drug resistance patients, as compared with K562 cells and CML patients. Upregulation of miR-3142 in K562 cells accelerated colony formation ability and enhanced resisitance to ADR in vitro. Conversely, inhibition of miR-3142 expression in K562/ADR cells decreased colony-formation ability and enhanced sensitivity to ADR in vitro and in vivo. Significantly, our results showed miR-3142-induced ADR resistance through targeting phosphatase and tensin homologue deleted on chromosome 10 (PTEN), which led to downregulation of PTEN protein and activation of PI3 kinase (PI3K)/Akt pathway. Inhibition of Akt using Akt inhibitor or introduction of PTEN largely abrogated miR-3142-induced resistance. These findings indicated that miR-3142 induces cell proliferation and ADR resistance primarily through targeting the PTEN/PI3K/Akt pathway and implicate the potential application of miR-3142 in cancer therapy.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: Functional screen analysis reveals miR-3142 as central regulator in chemoresistance and proliferation through activation of the PTEN-AKT pathway in CML

et al. 2017

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“…It was identified that miR-17 was downregulated in DDP-resistant NSCLC cells, which was consistent with results of a previous study (20). Furthermore, miR-17 is involved in modulating the cell viability and chemoresistance in a number of types of cancer, such as pancreatic and breast cancer (30,31). According to the bioinformatics software, there were binding sites between BLACAT1 and miR-17.…”

Section: Discussionsupporting

confidence: 88%

LncRNA BLACAT1 is involved in chemoresistance of non‑small cell lung cancer cells by regulating autophagy

Huang

Chen

Zheng³

et al. 2018

Int J Oncol

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The aim of the present study was to determine the effect of the long non-coding RNA (lncRNA) bladder cancer-associated transcript 1 (BLACAT1) in chemoresistance of non-small cell lung cancer (NSCLC) cells. Expression of lncRNA BLACAT1, microRNA (miR)-17, autophagy-related protein 7 (ATG7), multidrug-resistance protein 1 (MRP1), and the autophagy-associated proteins light chain 3 (LC3)-II/LC3-I and Beclin 1 were detected using the reverse transcription-quantitative polymerase chain reaction and western blot analysis. Cell viability was determined using an MTT assay. The interaction between BLACAT1 and miR-17 was determined using RNA immunoprecipitation and RNA pull-down assays. A cisplatin (DDP)-resistant NSCLC cell A549/DDP xenograft model in nude mice was established to investigate the effect of BLACAT1 on the chemoresistance of NSCLC cells. Compared with in DDP-sensitive NSCLC cells, expression of BLACAT1, ATG7, MRP1, LC3-II/LC3-I and Beclin 1 was significantly upregulated in DDP-resistant NSCLC cells, whereas miR-17 was downregulated in DDP-resistant NSCLC cells. Short interfering RNA against BLACAT1 decreased the viability of DDP-resistant NSCLC cells. In addition, BLACAT1 interacted with miR-17, and negatively regulated miR-17. BLACAT1 promoted ATG7 expression through miR-17, and facilitated autophagy and promoted chemoresistance of NSCLC cells through miR-17/ATG7. Finally, in vivo experiments indicated that inhibition of BLACAT1 ameliorated the chemoresistance of NSCLC. BLACAT1 was upregulated in DDP-resistant NSCLC cells, and promoted autophagy and chemoresistance of NSCLC cells through the miR-17/ATG7 signaling pathway.

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“…The well-known tumor suppressors PTEN, CNDK1A (p21), and ZBTB4 were reported to be critical targets of miR-17-5p. 42,46,47 Therefore, we further investigated the effects of PAX8-AS1-N on the expression of PTEN, CNDK1A, and ZBTB4. qRT-PCR assays revealed that enhanced PAX8-AS1-N expression upregulated PTEN, CNDK1A, and ZBTB4 mRNA levels ( Figure 6D).…”

Section: Cdkn1a and Zbtb4 Expression Via Interacting With Mir-17-5pmentioning

confidence: 99%

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

Cao

Tang

et al. 2018

J of Cellular Biochemistry

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Baicalein, a natural flavonoid, has fascinating anti-cancer properties in breast cancer. Long noncoding RNAs (lncRNAs), a class of transcripts with no protein-coding potential, also exhibit critical roles in breast cancer. However, the molecular mechanisms mediating the anti-cancer properties of baicalein and whether lncRNAs are involved in the anti-cancer effects are still unclear. In this study, we identified a novel isoform of lncRNA PAX8-AS1 (PAX8-AS1-N), which is activated by baicalein in a dose- and time-dependent manner. Functional assays showed that PAX8-AS1-N reduced cell viability, inhibited cell-cycle progression, and induced apoptosis of breast cancer cells in vitro. Depletion of PAX8-AS1-N promoted breast xenograft tumor growth in vivo. Furthermore, depletion of PAX8-AS1-N attenuated the suppressive roles of baicalein on cell viability, the apoptosis induced by baicalein, and also the suppressive roles of baicalein on tumor growth in vivo. Mechanistically, PAX8-AS1-N bound to miR-17-5p, and up-regulated miR-17-5p targets, such as PTEN, CDKN1A, and ZBTB4. In addition, PAX8-AS1-N was down-regulated in breast cancer and reduced expression of PAX8-AS1-N indicated poor survival of breast cancer patients. In conclusion, our results demonstrated that PAX8-AS1-N activation mediated the anti-cancer effects of baicalein via regulating miR-17-5p, and suggested that baicalein and enhancing PAX8-AS1-N would be potential therapeutic strategies against breast cancer.

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GFRα2 prompts cell growth and chemoresistance through down-regulating tumor suppressor gene PTEN via Mir-17-5p in pancreatic cancer

Cited by 56 publications

References 31 publications

RETRACTED ARTICLE: Functional screen analysis reveals miR-3142 as central regulator in chemoresistance and proliferation through activation of the PTEN-AKT pathway in CML

RETRACTED ARTICLE: Functional screen analysis reveals miR-3142 as central regulator in chemoresistance and proliferation through activation of the PTEN-AKT pathway in CML

LncRNA BLACAT1 is involved in chemoresistance of non‑small cell lung cancer cells by regulating autophagy

Baicalein inhibits breast cancer growth via activating a novel isoform of the long noncoding RNA PAX8‐AS1‐N

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