Suberoylanilide hydroxamic acid induces thioredoxin1‐mediated apoptosis in lung cancer cells via up‐regulation of miR‐129‐5p

You, Bo; Park, Woo Hyun

doi:10.1002/mc.22701

Cited by 31 publications

(12 citation statements)

References 48 publications

(116 reference statements)

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“…Ectopic expression of HIF1A-AS2 suppressed miR-129-5p expression in MG-63 cells. Several studies have suggested that miR-129-5p plays important roles in the development of tumors such as hepatocellular carcinoma, colon cancer, breast cancer, lung cancer, gastric cancer and osteosarcoma [43][44][45][46][47][48]. Long et al [48] showed that miR-129-5p expression might be regulated by demethylation and that miR-129-5p suppressed osteosarcoma cell invasion and migration by targeting valosin-containing protein (VCP) in osteosarcoma.…”

Section: Discussionmentioning

confidence: 99%

LncRNA HIF1A-AS2 promotes osteosarcoma progression by acting as a sponge of miR-129-5p

Wang

Peng

Gong

et al. 2019

Aging

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Increasing studies have demonstrated that long noncoding RNAs (lncRNAs) play vital roles in tumor development and progression. However, the relationship between osteosarcoma and HIF1AAS2 remains unknown. The expression of HIF1AAS2 and miR-129-5p was detected in osteosarcoma cell lines and samples via qRT-PCR. Cell Counting Kit-8 (CCK-8) and invasion assays were performed to determine cell proliferation and invasion ability, and a dual luciferase reporter assay was performed to determine the interaction between HIF1AAS2 and miR-129-5p. We showed that the expression of HIF1A-AS2 was upregulated in the osteosarcoma samples compared with the expression in noncancerous samples. Moreover, patients with high HIF1A-AS2 expression had a shorter overall survival. Ectopic expression of HIF1A-AS2 enhanced osteosarcoma cell proliferation, cell cycle progression and invasion. We found that overexpression of miR-129-5p decreased the luciferase activity of wild-type (WT) HIF1A-AS2 but not mutant HIF1A-AS2. Ectopic expression of HIF1A-AS2 suppressed miR-129-5p expression in MG-63 cells. We demonstrated that miR-129-5p was downregulated in osteosarcoma and was negatively associated with HIF1A-AS2 expression. Furthermore, ectopic expression of miR-129-5p suppressed osteosarcoma cell proliferation, cell cycle progression and invasion. In addition, overexpression of HIF1A-AS2 promoted cell proliferation, cell cycle progression and invasion of osteosarcoma cells through the modulation of miR-129-5p. These results indicated that HIF1A-AS2 might be a potential therapeutic target for osteosarcoma.

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Section: Discussionmentioning

confidence: 99%

LncRNA HIF1A-AS2 promotes osteosarcoma progression by acting as a sponge of miR-129-5p

Wang

Peng

Gong

et al. 2019

Aging

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“…HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), have been shown to induce apoptosis in various cancer cells by increasing the production of ROS [188,189]. You et al [190] found that miR-129-5p was upregulated by SAHA-treatment in cancer cells and, at least in part, mediated ROS increased production by targeting the antioxidant protein thioredoxin1 (Trx1). More recently and in line with this, miR-129-5p has been shown to function as a tumor suppressor when overexpressed in lung cancer cells [191].…”

Section: Mir-155 and Oxidative Stress In Cardiac And Pulmonary Diseasesmentioning

confidence: 99%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

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Reactive oxygen species (ROS) affect many cellular functions and the proper redox balance between ROS and antioxidants contributes substantially to the physiological welfare of the cell. During pathological conditions, an altered redox equilibrium leads to increased production of ROS that in turn may cause oxidative damage. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level contributing to all major cellular processes, including oxidative stress and cell death. Several miRNAs are expressed in response to ROS to mediate oxidative stress. Conversely, oxidative stress may lead to the upregulation of miRNAs that control mechanisms to buffer the damage induced by ROS. This review focuses on the complex crosstalk between miRNAs and ROS in diseases of the cardiac (i.e., cardiac hypertrophy, heart failure, myocardial infarction, ischemia/reperfusion injury, diabetic cardiomyopathy) and pulmonary (i.e., idiopathic pulmonary fibrosis, acute lung injury/acute respiratory distress syndrome, asthma, chronic obstructive pulmonary disease, lung cancer) compartments. Of note, miR-34a, miR-144, miR-421, miR-129, miR-181c, miR-16, miR-31, miR-155, miR-21, and miR-1/206 were found to play a role during oxidative stress in both heart and lung pathologies. This review comprehensively summarizes current knowledge in the field.

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“…With the deepening of miRNA research, targeting their downstream genes to regulate multidrug resistance has become a research hotspot. MiR-129-5p, a tumor inhibitor, has been validated to inhibit cancer cells migration, proliferation, differentiation, and epithelial-mesenchymal transition (17 –20). In addition, miR-129-5p-mediated beclin-1 suppression inhibits endothelial cell autophagy in atherosclerosis (21).…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-129-5p increases the sensitivity to Taxol through inhibiting HMGB1-mediated cell autophagy in breast cancer MCF-7 cells

Shi

Gong

et al. 2019

Braz J Med Biol Res

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Although Taxol has improved the survival of cancer patients as a first-line chemotherapeutic agent, an increasing number of patients develop resistance to Taxol after prolonged treatment. The potential mechanisms of cancer cell resistance to Taxol are not completely clear. It has been reported that microRNAs (miRNAs) are involved in regulating the sensitivity of cancer cells to various chemotherapeutic agents. In this study, we aimed to explore the role of miR-129-5p in regulating the sensitivity of breast cancer cells to Taxol. Cell apoptosis and autophagy, and the sensitivity of MCF-7 cells to Taxol were assessed with a series of in vitro assays. Our results showed that the inhibition of autophagy increased the Taxol-induced apoptosis and the sensitivity of MCF-7 cells to Taxol. Up-regulation of miR-129-5p also inhibited autophagy and induced apoptosis. Furthermore, miR-129-5p overexpression increased the sensitivity of MCF-7 cells to Taxol. High mobility group box 1 (HMGB1), a target gene of miR-129-5p and a regulator of autophagy, was negatively regulated by miR-129-5p. We found that interference of HMGB1 enhanced the chemosensitivity of Taxol by inhibiting autophagy and inducing apoptosis in MCF-7 cells. Taken together, our findings suggested that miR-129-5p increased the chemosensitivity of MCF-7 cells to Taxol through suppressing autophagy and enhancing apoptosis by inhibiting HMGB1. Using miR-129-5p/HMGB1/autophagy-based therapeutic strategies may be a potential treatment for overcoming Taxol resistance in breast cancer.

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Suberoylanilide hydroxamic acid induces thioredoxin1‐mediated apoptosis in lung cancer cells via up‐regulation of miR‐129‐5p

Cited by 31 publications

References 48 publications

LncRNA HIF1A-AS2 promotes osteosarcoma progression by acting as a sponge of miR-129-5p

LncRNA HIF1A-AS2 promotes osteosarcoma progression by acting as a sponge of miR-129-5p

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Upregulation of miR-129-5p increases the sensitivity to Taxol through inhibiting HMGB1-mediated cell autophagy in breast cancer MCF-7 cells

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