MiR-654-3p targets SRC to suppress tumor growth in non-small cell lung cancer

Pang, Mei-Yan; Jiang, Yongjie; Huang, Yuyan; Ren, Bing; He, Leiyan; Li, Jiang

doi:10.14715/cmb/2023.69.4.25

Cell Mol Biol (Noisy-le-grand)

2023

DOI: 10.14715/cmb/2023.69.4.25

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MiR-654-3p targets SRC to suppress tumor growth in non-small cell lung cancer

Mei-Yan Pang¹,

Yongjie Jiang²,

Yuyan Huang³

et al.

Abstract: Materials and Methods Cell linesHuman lung cancer cell lines (A549, H1299, SK-MES-1) and normal lung epithelial cells (BEAS-2B) were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China) and cultured in F-12K, RPMI-1640 and MEM medium (Procell, Wuhan, China) respectively, with 10% fetal bovine serum (Procell, Wuhan, China) and 100 U/ml penicillin and 100 µg/ml streptomycin (Procell, Wuhan, China) at 37°C with 5% CO2. Cell transfection and infectionH1299 cells were transfected with miR-654-3… Show more

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2024

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Cited by 2 publications

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To investigate the role and potential mechanism of has_circ_RBMS3 in bone metastasis of breast cancer based on bioinformatics

Long,

Tan

2024

Cell Biochem Biophys

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To investigate the role and potential mechanism of has_circ_RBMS3 in bone metastasis of breast cancer based on bioinformatics

Long,

Tan

2024

Cell Biochem Biophys

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Pyroptosis and mitochondrial function participated in miR-654-3p-protected against myocardial infarction

Wu,

Zhang,

Chen

et al. 2024

Cell Death Dis

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Myocardial infarction (MI) is one of the leading causes of heart failure with highly complicated pathogeneses. miR-654-3p has been recognized as a pivotal regulator of controlling cell survival. However, the function of miR-654-3p in cardiomyocytes and MI has yet to be reported. This study aimed to identify the role of miR-654-3p in the regulation of myocardial infarction. To understand the contribution of miR-654-3p on heart function, we generated cardiac-specific knockdown and overexpression mice using AAV9 technology in MI injury. Mechanically, we combined cellular and molecular techniques, pharmaceutical treatment, RNA sequencing, and functional testing to elucidate the potential pathological mechanisms. We identified that mice subjected to MI decreased the expression of miR-654-3p in the border and infarcted area. Mice lacking miR-654-3p in the heart showed some inflammation infiltration and myocardial fibrosis, resulting in a mild cardiac injury. Furthermore, we found a deficiency of miR-654-3p in cardiomyocytes resulted in pyroptotic cell death but not other programmed cell death. Intriguingly, miR-654-3p deficiency aggravated MI-induced cardiac dysfunction, accompanied by higher myocardial fibrosis and cardiac enzymes and augmented pyroptosis activation. Cardiac elevating miR-654-3p prevented myocardial fibrosis and inflammation infiltration and decreased pyroptosis profile, thereby attenuating MI-induced cardiac damage. Using RNA sequence and molecular biological approaches, we found overexpression of miR-654-3p in the heart promoted the metabolic ability of the cardiomyocytes by promoting mitochondrial metabolism and mitochondrial respiration function. Our finding identified the character of miR-654-3p in protecting against MI damage by mediating pyroptosis and mitochondrial metabolism. These findings provide a new mechanism for miR-654-3p involvement in the pathogenesis of MI and reveal novel therapeutic targets.

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MiR-654-3p targets SRC to suppress tumor growth in non-small cell lung cancer

Cited by 2 publications

References 26 publications

To investigate the role and potential mechanism of has_circ_RBMS3 in bone metastasis of breast cancer based on bioinformatics

To investigate the role and potential mechanism of has_circ_RBMS3 in bone metastasis of breast cancer based on bioinformatics

Pyroptosis and mitochondrial function participated in miR-654-3p-protected against myocardial infarction

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