Metformin, an ancient drug commonly used for treating type II diabetes, has been associated to anti-cancer capacity in a variety of developing cancers, though the mechanism remains elusive. Here, we aimed to examine the inhibitory effect of metformin in osteosarcoma. Herein, we demonstrated that metformin treatment blocked proliferation progression by causing accumulation of G2/M phase in U2OS and 143B cells. Furthermore, metformin treatment triggered programmed cell death process in osteosarcoma cell lines. Further research indicated the induction of apoptosis and autophagy triggered by metformin could remarkably attenuate after the treatment of ROS scavenger NAC and JNK inhibitor SP600125. Additionally, our results showed that NAC-suppressed JNK/c-Jun signaling pathway could have been activated through metformin treatment. Lastly, metformin could inhibit osteosarcoma growth under safe dose . Thus, we propose that metformin could induce cell cycle arrest as well as programmed cell death, including apoptosis and autophagy, through ROS-dependent JNK/c-Jun cascade in human osteosarcoma. This metformin-induced pathway provides further insights into its antitumor potential molecular mechanism and illuminates potential cancer targets for osteosarcoma.
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http://dx.doi.org/10.7150/ijbs.33787 | DOI Listing |
Mol Neurobiol
December 2024
Department of Biochemistry and Molecular Biology, Harbin Medical University, Harbin, 150000, Heilongjiang, China.
Ferroptosis and autophagy are closely associated with Alzheimer's disease (AD). Elevated ferric ion levels can induce oxidative stress and chronic inflammatory responses, resulting in brain tissue damage and further neurological cell damage. Autophagy in Alzheimer's has a dual role.
View Article and Find Full Text PDFJ Adv Res
December 2024
Department of Pathology, Xuzhou Medical University, Xuzhou, China. Electronic address:
The cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway has been identified as a crucial mechanism in antiviral defense and innate immunity pathway. Ferroptosis, characterized by iron dependence and lipid peroxidation, represents a specialized form of cell death. A burgeoning collection of studies has demonstrated that the cGAS-STING signaling pathway participates in the homeostatic regulation of the organism by modulating ferroptosis-associated enzyme activity or gene expression.
View Article and Find Full Text PDFEur J Pharmacol
December 2024
School of Pharmacy, Bengbu Medical University, Bengbu, China; Anhui Province Engineering Technology Research Center of Biochemical Pharmaceutical, Bengbu, China. Electronic address:
In recent decades, significant advancements have been achieved in non-small cell lung cancer (NSCLC) treatment. However, drug resistance, postoperative recurrence, distant metastasis, and other critical issues arise during NSCLC treatment. Natural products play a crucial role in the development of anti-tumor drugs.
View Article and Find Full Text PDFBiochem Pharmacol
December 2024
Department of Orthopedics, The First Affiliated Hospital of Soochow University, Suzhou 215006, Jiangsu, China. Electronic address:
As an important pathological process, annulus fibrosus (AF) degeneration contributes greatly to intervertebral disc degeneration (IVDD). Moreover, extracellular matrix (ECM) degradation and AF cell (AFC) autophagy are of utmost importance. The involvement of cannabinoid receptor type 2 (CB2) in the pathological mechanisms underlying different diseases has been demonstrated dueto its capacity toregulateautophagy.
View Article and Find Full Text PDFBrain Res
December 2024
Department of Neurology, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, Guangxi, China; Key Laboratory of Research on Clinical Molecular Diagnosis for High Incidence Diseases in Western Guangxi of Guangxi Higher Education Institutions, Baise, Guangxi, China. Electronic address:
This study aimed to investigate the impact of chronic cerebral hypoperfusion (CCH) on cognitive function, amyloid-β (Aβ) deposition, cellular autophagy, and mitochondrial dynamics in an Alzheimer's disease (AD) mouse model, and to evaluate the intervention effects of autophagy modulation on these outcomes. Utilizing the APP/PS1 mouse model combined with CCH, we assessed cognitive function, Aβ deposition, and the expression levels of relevant proteins through behavioral tests and immunohistochemical analysis. Our findings revealed pronounced cognitive deficits and increased Aβ deposition in the AD + CCH group mice, along with upregulation of mitochondrial fission proteins (Drp1, Fis1) and downregulation of mitochondrial fusion proteins (Opa1, Mfn1), indicating a shift towards mitochondrial fission and promoting cell apoptosis.
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