miRNA 146a promotes chemotherapy resistance in lung cancer cells by targeting DNA damage inducible transcript 3 (CHOP)

Tan, Wenfeng; Liao, Yi; Yang, Qin; Liu, Hongxiang; Tan, Deli; Wu, Tao; Tang, Meng; Zhang, Shixin; Wang, Haidong

doi:10.1016/j.canlet.2018.04.028

Cited by 53 publications

(55 citation statements)

References 33 publications

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“…In this study, we constructed a drug‐resistant lung adenocarcinoma cell line A549/CDDP. Consistent with our previously report, the IC 50 of A549/CDDP cells was significantly enhanced . Interestingly, we found that the IC 50 of parental A549 cells which we used in this study was significantly higher than that reported in our previous study, while the IC 50 of A549/CDDP cell lines was lower than that reported in previously study .…”

Section: Discussionsupporting

confidence: 91%

“…Consistent with our previously report, the IC 50 of A549/CDDP cells was significantly enhanced . Interestingly, we found that the IC 50 of parental A549 cells which we used in this study was significantly higher than that reported in our previous study, while the IC 50 of A549/CDDP cell lines was lower than that reported in previously study . We suspect that it may be the parental A549 cells accumulating resistance‐related mutations during continuous passage, such as ROS mutations, resulting in differences in drug sensitivity of the same cell line.…”

Section: Discussionsupporting

confidence: 90%

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IL‐25 promotes cisplatin resistance of lung cancer cells by activating NF‐κB signaling pathway to increase of major vault protein

Shen

Yang

et al. 2019

Cancer Medicine

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As an inflammatory factor, IL‐25 has been studied in variouscancers, but it is rarely reported in cancer chemotherapy resistance. Major vault protein (MVP), as a gene associated with lung multidrug resistance, is associated with multiple chemotherapy resistances of lung cancer. However, the relationship between IL‐25 and MVP in lung cancer cells has not been studied. In this study, we found that both IL‐25 and MVP were elevated expressed in cisplatin‐resistant lung adenocarcinoma cell line (A549/CDDP). Silencing of IL‐25 resulted in down‐regulation of MVP expression and reduced cisplatin tolerance of A549/CDDP cells. Overexpression of IL‐25 resulted in increase of MVP expression and the cisplatin tolerance in A549 cells. In addition, we found that the extracellular IL‐25 could stimulate the expression of MVP and activate the NF‐κB signaling pathway. Further, animal models also confirmed that IL‐25 reduced the sensitivity of xenografts to chemotherapy. Taken together, we believe that the up‐regulation of IL‐25 induces MVP expression contributing to chemotherapy resistances of lung cancer cells. Our findings suggest that interference the expression of IL‐25 might be potential treatment strategies for the clinical reversing the chemotherapy resistance.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionsupporting

confidence: 90%

IL‐25 promotes cisplatin resistance of lung cancer cells by activating NF‐κB signaling pathway to increase of major vault protein

Shen

Yang

et al. 2019

Cancer Medicine

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“…[31] In CHOP À/À rats and CHOP-silenced cells, cell apoptosis induced by ERS was decreased. [32,33] In this study, the activation capacity of PERK protein was enhanced, and the expression levels of ATF-4 and CHOP protein were upregulated in SHRs, indicating that cardiomyocyte apoptosis caused by ERS via activating PERK. IRSII could weaken the phosphorylation capacity of PERK and reduce the expression of ATF-4 and CHOP protein, signifying its inhibitory effect on PERK signalling pathway.…”

Section: Discussionmentioning

confidence: 52%

“…The principal apoptosis‐promoting transcription factor is CHOP, which is an ERS‐specific transcription factor and plays a central role in cell apoptosis induced by ERS . In CHOP −/− rats and CHOP‐silenced cells, cell apoptosis induced by ERS was decreased . In this study, the activation capacity of PERK protein was enhanced, and the expression levels of ATF‐4 and CHOP protein were upregulated in SHRs, indicating that cardiomyocyte apoptosis caused by ERS via activating PERK.…”

Section: Discussionmentioning

confidence: 53%

Icariside II prevents hypertensive heart disease by alleviating endoplasmic reticulum stress via the PERK/ATF-4/CHOP signalling pathway in spontaneously hypertensive rats

Yue

et al. 2019

Journal of Pharmacy and Pharmacology

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Objectives Reducing endoplasmic reticulum stress (ERS)‐induced cardiomyocyte apoptosis is a key strategy for preventing hypertensive heart disease. In our previous study, Icariside II can improve left ventricular remodelling in spontaneously hypertensive rats (SHRs). This study aims to determine whether Icariside II can exert its effect by inhibiting ERS‐induced cardiomyocyte apoptosis via the PERK/ATF‐4/CHOP signalling pathway. Methods Spontaneously hypertensive rats were randomly divided into model group and Icariside II groups. The rats in the Icariside II groups were intragastrically administrated with Icariside II 4, 8 and 16 mg/kg from 14 to 26 week‐age, respectively. The left ventricular function was measured at the 18, 22 and 26 week‐age by small animal ultrasound. At the end of the 26th week, cardiomyocyte apoptosis was analysed and the levels of GRP78, PERK, ATF‐4 and CHOP gene and protein were detected. Key findings The function of left ventricular became declined with age in SHRs, but improved in Icariside II groups. Myocardial apoptosis was aggravated in SHRs, but alleviated in Icariside II groups. Icariside II could reduce the levels of GRP78, PERK, ATF‐4, CHOP gene and protein that increased in SHRs. Conclusions Icariside II prevents hypertensive heart disease by alleviating ERS‐induced cardiomyocyte apoptosis, and its mechanism is related to the impediment of the PERK/ATF‐4/CHOP signalling pathway.

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“…As miRNA regulation can alter the expression of resistance‐related genes, abnormal expression of miRNAs can also induce drug resistance in cancer 16 . Furthermore, miRNAs play a critical role in the differentiation and self‐renewal of CSCs 17 . For instance, miR‐5100 promotes the self‐renewal and cisplatin resistance of lung CSCs by targeting Ras‐related protein 6 18 …”

Section: Introductionmentioning

confidence: 99%

miR‐155 increases stemness and decitabine resistance in triple‐negative breast cancer cells by inhibiting TSPAN5

Yang

Xian-jin

Liang

et al. 2020

Molecular Carcinogenesis

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Effective therapeutic targets for triple‐negative breast cancer (TNBC), a special type of breast cancer (BC) with rapid metastasis and poor prognosis, are lacking, especially for patients with chemotherapy resistance. Decitabine (DCA) is a Food and Drug Administration‐approved DNA methyltransferase inhibitor that has been proven effective for the treatment of tumors. However, its antitumor effect in cancer cells is limited by multidrug resistance. Cancer stem cells (CSCs), which are thought to act as seeds during tumor formation, regulate tumorigenesis, metastasis, and drug resistance through complex signaling. Our previous study found that miR‐155 is upregulated in BC, but whether and how miR‐155 regulates DCA resistance is unclear. In this study, we demonstrated that miR‐155 was upregulated in CD24−CD44+ BC stem cells (BCSCs). In addition, the overexpression of miR‐155 increased the number of CD24−CD44+ CSCs, DCA resistance and tumor clone formation in MDA‐231 and BT‐549 BC cells, and knockdown of miR‐155 inhibited DCA resistance and stemness in BCSCs in vitro. Moreover, miR‐155 induced stemness and DCA resistance by inhibiting the direct target gene tetraspanin‐5 (TSPAN5). We further confirmed that overexpression of TSPAN5 abrogated the effect of miR‐155 in promoting stemness and DCA resistance in BC cells. Our data show that miR‐155 increases stemness and DCA resistance in BC cells by targeting TSPAN5. These data provide a therapeutic strategy and mechanistic basis for future possible clinical applications targeting the miR‐155/TSPAN5 signaling axis in the treatment of TNBC.

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miRNA 146a promotes chemotherapy resistance in lung cancer cells by targeting DNA damage inducible transcript 3 (CHOP)

Cited by 53 publications

References 33 publications

IL‐25 promotes cisplatin resistance of lung cancer cells by activating NF‐κB signaling pathway to increase of major vault protein

IL‐25 promotes cisplatin resistance of lung cancer cells by activating NF‐κB signaling pathway to increase of major vault protein

Icariside II prevents hypertensive heart disease by alleviating endoplasmic reticulum stress via the PERK/ATF-4/CHOP signalling pathway in spontaneously hypertensive rats

miR‐155 increases stemness and decitabine resistance in triple‐negative breast cancer cells by inhibiting TSPAN5

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