Chidamide-induced ROS accumulation and miR-129-3p-dependent cell cycle arrest in non-small lung cancer cells

Wu, Yueh-Feng; Ou, Chu‐Chyn; Chien, Peng-Ju; Chang, Haṡok; Ko, Jiunn‐Liang; Wang, Bing‐Yen

doi:10.1016/j.phymed.2018.09.218

Cited by 27 publications

(23 citation statements)

References 37 publications

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“…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]. Furthermore, chidamide, an oral benzamide-type selective HDAC inhibitor, has been shown to induce cancer cell cycle arrest by inducing upregulation of miR-129-3p together with ROS production to inhibit telomerase activity [192].…”

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

confidence: 84%

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

confidence: 84%

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Climent

Viggiani

Lin

et al. 2020

IJMS

View full text Add to dashboard Cite

show abstract

“…He et al, 2012 have demonstrated that via epigenetic mechanisms, ROS decreases miR-199a and miR-125b expression in ovarian cancer cells, through the promoter methylation of miR-199a and miR-125b [201]. It was also documented that Chidamide, a HDAC inhibitor (HDACi), increased ROS production in cells and up-regulated miR-129-3p expression in H1355 and A549 lung adenocarcinoma cells [202]. In cells, Chidamide suppressed telomerase activity through ROS accumulation and cell cycle arrest.…”

Section: Role Of Ros In Cancer Cell Killingmentioning

confidence: 99%

Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements

et al. 2019

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Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.

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“…Chidamide, an inhibitor of the enzyme histone deacetylase, was shown to decrease telomerase expression through miR-129-3p up-regulation in non-small cell lung cancer cells. This leads to subsequent ROS accumulation and subsequent cell cycle arrest ( 213 ). Epigenetic mechanisms may also be exploited in potential therapies using personalized approach.…”

Section: Tert As a Potential Therapeutic Targetmentioning

confidence: 99%

TERT—Regulation and Roles in Cancer Formation

et al. 2020

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Telomerase reverse transcriptase (TERT) is a catalytic subunit of telomerase. Telomerase complex plays a key role in cancer formation by telomere dependent or independent mechanisms. Telomere maintenance mechanisms include complex TERT changes such as gene amplifications, TERT structural variants, TERT promoter germline and somatic mutations, TERT epigenetic changes, and alternative lengthening of telomere. All of them are cancer specific at tissue histotype and at single cell level. TERT expression is regulated in tumors via multiple genetic and epigenetic alterations which affect telomerase activity. Telomerase activity via TERT expression has an impact on telomere length and can be a useful marker in diagnosis and prognosis of various cancers and a new therapy approach. In this review we want to highlight the main roles of TERT in different mechanisms of cancer development and regulation.

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Chidamide-induced ROS accumulation and miR-129-3p-dependent cell cycle arrest in non-small lung cancer cells

Cited by 27 publications

References 37 publications

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

MicroRNA and ROS Crosstalk in Cardiac and Pulmonary Diseases

Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements

TERT—Regulation and Roles in Cancer Formation

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