MiR-204 reduces cisplatin resistance in non-small cell lung cancer through suppression of the caveolin-1/AKT/Bad pathway

Huang, Gang; Lou, Tianzheng; Pan, Jiongwei; Ye, Zaiting; Yin, Zhangyong; Li, Lü; Cheng, Wei; Cao, Zhuo

doi:10.18632/aging.101907

Cited by 21 publications

(18 citation statements)

References 41 publications

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“…To further confirm and validate a link between miR204-5p expression and CAV-1 expression, we demonstrated that transfection of A549 and NCI-H460 cells with a specific miR204-5p inhibitor (prior to TL treatment) effectively repressed the TL-induced inhibitory effect on Cav-1 mRNA transcript expression ( Figure 5A). These findings are consistent with reports of Cav-1 being a target of miR204-5p [17,[41][42][43][44]. More specifically, our data substantiate very recent findings by Huang et al [44] that downregulation of miR-204 expression is responsible for CAV-1 overexpression in cisplatin-resistant A549 cells.…”

Section: Discussionsupporting

confidence: 94%

“…These findings are consistent with reports of Cav-1 being a target of miR204-5p [17,[41][42][43][44]. More specifically, our data substantiate very recent findings by Huang et al [44] that downregulation of miR-204 expression is responsible for CAV-1 overexpression in cisplatin-resistant A549 cells. Taken together, our findings indicate that: 1) Cav-1 is a likely target of miR204-5p and 2) miR204-5p plays a key role in TL-induced down-regulation of Cav-1/Sirt-1/-3 in A549 and NCI-H460 NSCLC cells.…”

Section: Discussionsupporting

confidence: 94%

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Triptolide-induced apoptosis in non-small cell lung cancer via a novel miR204-5p/Caveolin-1/Akt-mediated pathway

et al. 2020

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Lung cancer is one of the most prevalent malignancies worldwide with non-small cell lung cancer (NSCLC) comprising nearly 80% of all cases. Unfortunately, many lung cancer patients are diagnosed at advanced stages of the disease with an associated poor prognosis. Recently, the Chinese herb root extract Triptolide/Minnelide (TL) has shown significant promise as a therapeutic agent for NSCLC treatment both in vitro and in vivo. The aim of this study was to investigate the underlying mechanism(s) of action regarding TL-induced cytotoxicity in NSCLC. We demonstrate that triptolide treatment of A549 and H460 NSCLC cells decreases Caveolin-1 (CAV-1) mRNA/protein expression, resulting in activation of the Akt/Bcl-2-mediated mitochondrial apoptosis pathway. CAV-1 down-regulation was triggered by Micro-RNA 204-5p (miR204-5p) up-regulation and could be significantly blocked by pre-treatment with both Sirt-1/ Sirt-3 specific siRNA and SIRT-1/SIRT-3 enzyme inhibitors, EX-527 and nicotinamide. Overall, our results provide evidence for a novel mechanism by which TL exerts its cytotoxic effects on NSCLC via CAV-1 down-regulation. Furthermore, these findings demonstrate a pivotal role for TL induction of the Akt/Bax pathway in apoptosis of human lung cancer.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionsupporting

confidence: 94%

Triptolide-induced apoptosis in non-small cell lung cancer via a novel miR204-5p/Caveolin-1/Akt-mediated pathway

et al. 2020

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“…MiRs are endogenous non-coding RNA, existed in eukaryotic cells to suppressed genes expression on the transcriptional level and play the part of cancer gene or antioncogene [9]. MiR-204 is ordinarily poorly expressed in multiple cancers, and pose as a tumor inhibitor in cancers [10]. It has been suggested that by regulating miR-204-3p and inhibiting autophagy, downregulated expression of lncRNA AK139328 alleviated myocardial I/R injury in glycuresis mice [11].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: LncRNA HIF1A-AS1 contributes to ventricular remodeling after myocardial ischemia/reperfusion injury by adsorption of microRNA-204 to regulating SOCS2 expression

Xue

Luo

2019

Cell Cycle

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Objectives: Long non-coding RNAs (lncRNAs) serve pivotal roles in heart disease, while the role of lncRNA hypoxia-inducible factor 1α-antisense RNA 1 (HIF1A-AS1) is rarely mentioned. Therefore, the objective of this study was to investigate the mechanism of lncRNA HIF1A-AS1 regulating suppressor of cytokine signaling 2 (SOCS2) expression by adsorption of microRNA-204 (miR-204) on ventricular remodeling after myocardial ischemia-reperfusion (I/R) injury in mice. Methods: The mouse model of I/R was established by left coronary artery occlusion. The expression of HIF1A-AS1, miR-204 and SOCS2 was determined. The mice were injected with HIF1A-AS1-siRNA, miR-204 mimics or their controls to investigate their effects on cardiac function and ventricular remodeling of mice after I/R injury. The binding relationship between HIF1A-AS1 and miR-204 as well as between miR-204 and SOCS2 were verified. Results: HIF1A-AS1 and SOCS2 were upregulated and miR-204 was downregulated in myocardial tissues in mice after I/R injury. LVEDD, LVEDS, LVEDP, LVMI and RVMI expression reduced while LVEF, LVFS, +dp/dt max anddp/dt max increased through knockdown HIF1A-AS1 and upregulated miR-204. The expression of BNP, cTnI, LDH, CK, TNF-α, IL-1β, IL-6 and β-MHC reduced, and the expression of α-MHC increased when HIF1A-AS1 was poorly expressed and miR-204 was highly expressed. Silencing HIF1A-AS1 and upregulating miR-204 inhibited apoptosis of cells. LncRNA HIF1A-AS1 could act as ceRNA to adsorb miR-204 to suppress miR-204 expression and elevate SOCS2 expression. Conclusion: Our study provides evidence that downregulation of HIF1A-AS1 and upregulation of miR-204 could alleviate ventricular remodeling and improve cardiac function in mice after myocardial I/R injury via regulating SOCS2.

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“…In A549 and PC-9 cells, Cav-1 expression can be negatively modulated by its upstream regulator miR-204. The phosphorylation of AKT and Bad can be further suppressed by the miR-204/Cav-1 pathway, which can promote cisplatin-induced apoptosis by silencing Bcl-2 and Bcl-xl, indicating the positive role of Cav-1 during this process [105]. In paclitaxel-resistant A549 cells, Cav-1 knockdown upregulates Bax, caspase-3 and caspase-9, and downregulates Bcl-2, finally prompting cell apoptosis [49].…”

Section: Roles Of Cav-1 In Programmed Cell Deathmentioning

confidence: 99%

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

Shi

Lai

et al. 2020

Cancers

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Lung cancer is one of the most common and malignant cancers with extremely high morbidity and mortality in both males and females. Although traditional lung cancer treatments are fast progressing, there are still limitations. Caveolin-1 (Cav-1), a main component of caveolae, participates in multiple cellular events such as immune responses, endocytosis, membrane trafficking, cellular signaling and cancer progression. It has been found tightly associated with lung cancer cell proliferation, migration, apoptosis resistance and drug resistance. In addition to this, multiple bioactive molecules have been confirmed to target Cav-1 to carry on their anti-tumor functions in lung cancers. Cav-1 can also be a predictor for lung cancer patients’ prognosis. In this review, we have summarized the valuable research on Cav-1 and lung cancer in recent years and discussed the multifaceted roles of Cav-1 on lung cancer occurrence, development and therapy, hoping to provide new insights into lung cancer treatment.

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MiR-204 reduces cisplatin resistance in non-small cell lung cancer through suppression of the caveolin-1/AKT/Bad pathway

Cited by 21 publications

References 41 publications

Triptolide-induced apoptosis in non-small cell lung cancer via a novel miR204-5p/Caveolin-1/Akt-mediated pathway

Triptolide-induced apoptosis in non-small cell lung cancer via a novel miR204-5p/Caveolin-1/Akt-mediated pathway

RETRACTED ARTICLE: LncRNA HIF1A-AS1 contributes to ventricular remodeling after myocardial ischemia/reperfusion injury by adsorption of microRNA-204 to regulating SOCS2 expression

Multifaceted Roles of Caveolin-1 in Lung Cancer: A New Investigation Focused on Tumor Occurrence, Development and Therapy

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