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Commentary: Lico A causes ER stress and apoptosis via up-regulating miR-144-3p in human lung cancer cell line H292.

ABSTRACT: Natural compound licochalcone A (lico A), a main constituent of flavonoids, has been proved to induce ER stress and apoptosis in cancer cells. However, the underlying anti-tumor mechanism of lico A remains to be clarified in detail. A recently-published report from the journal Frontiers in Pharmacology evaluated the miRNA-based mechanism for lico A on its anti-cancer effect. They found that lico A significantly promoted the tumor-suppressor miR-144-3p expression, so as to up-regulate ER stress-response protein CHOP (CCAAT/-enhancer-binding protein homologous protein) by down-regulating nuclear factor E2-related factor 2 (Nrf2), finally inducing apoptotic cell death in lung cancer. Their findings pave the path toward a more understanding of miRNA-based drugs for cancer treatment in the future.

SUBMITTER: Yan Y

PROVIDER: S-EPMC6362273 | biostudies-literature | 2018 Dec

REPOSITORIES: biostudies-literature

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Commentary: Lico A causes ER stress and apoptosis via up-regulating miR-144-3p in human lung cancer cell line H292.

Yan Yuanliang Y Gong Zhicheng Z Xu Zhijie Z

Biomedical journal 20181201 6

Natural compound licochalcone A (lico A), a main constituent of flavonoids, has been proved to induce ER stress and apoptosis in cancer cells. However, the underlying anti-tumor mechanism of lico A remains to be clarified in detail. A recently-published report from the journal Frontiers in Pharmacology evaluated the miRNA-based mechanism for lico A on its anti-cancer effect. They found that lico A significantly promoted the tumor-suppressor miR-144-3p expression, so as to up-regulate ER stress-r ...[more]

PMID: 30709582

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Project description:Autophagy and apoptosis are associated with cardiovascular diseases. Emerging evidence shows that microRNAs (miRs) are critical in the development of pathological processes underlying cardiovascular diseases by regulating the induction of apoptosis and autophagy. The present study aimed to investigate the role of miR‑103a‑3p in cardiomyocyte injury through autophagy and apoptosis. H9c2 cells were cultured under hypoxia and reoxygenation (H/R) conditions and were used to mimic cells under ischemia. The transfection of cells with miR‑103a‑3p (mimics and inhibitors) was performed to examine its function in cardiomyocytes. The expression levels of miR‑103a‑3p were evaluated by reverse transcription‑quantitative polymerase chain reaction analysis. Cell viability was determined using an MTT assay, and the lactate dehydrogenase assay (LDH) was used to investigate cell injury. The expression levels of B‑cell lymphoma 2 (Bcl‑2), Bcl‑2‑associated X protein, Beclin‑1, autophagy‑related 5 (Atg5), cleaved caspase‑3 and cleaved caspase‑9 were detected using western blotting. Immunofluorescence assays were performed to detect the expression of LC3 as a marker of autophagy. The target gene of miR‑103a‑3p was identified using dual‑luciferase reporter assays. The results revealed that the expression levels of miR‑103a‑3p were significantly downregulated in cardiomyocytes under H/R conditions. Injury of the cardiomyocytes was evaluated under H/R conditions. Following transfection of the cells with miR‑103a‑3p inhibitors, cell injury was increased, as determined by LDH and MTT assays. The expression levels of apoptotic proteins were consistent with the results obtained in the LDH and cell viability assays. The induction of autophagy was increased in cells under H/R conditions and cells with miR‑103a‑3p inhibitor transfection, whereas the induction of autophagy was decreased in cells transfected with miR‑103a‑3p mimics. In addition, the data indicated that miR‑103a‑3p directly targeted Atg5, which regulated the induction of autophagy and apoptosis. Taken together, these findings indicate that, following the inhibition of miR‑103a‑3p, Atg5 promotes autophagy and apoptosis in cardiomyocytes by directly targeting Atg5. Therefore, miR‑103a‑3p can be considered a potential therapeutic target for myocardial ischemia.

Dataset Information

Commentary: Lico A causes ER stress and apoptosis via up-regulating miR-144-3p in human lung cancer cell line H292.

Publications

Commentary: Lico A causes ER stress and apoptosis via up-regulating miR-144-3p in human lung cancer cell line H292.

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