Sodium cantharidinate suppresses human osteosarcoma MG‑63 cell proliferation and induces cell cycle arrest by inhibition of PI3K/AKT activation

Kong, Daliang; Liu, Yang; Wang, Jingying; Gong, Li; Zhang, Minglei

doi:10.3892/or.2018.6906

Cited by 6 publications

(7 citation statements)

References 24 publications

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“…OS is a common malignant tumor occurs in children as well as adolescents with a reduced prognosis. The currently existing treatments for OS leftovers unacceptable because of the higher side effects and development of resistance towards chemo and radiotherapy ( Kong et al, 2019 , Goudarzi et al, 2014 ). Furthermore, continued administration of the same medical interventions could directs to the tumor resistance.…”

Section: Discussionmentioning

confidence: 99%

Dieckol exerts anticancer activity in human osteosarcoma (MG-63) cells through the inhibition of PI3K/AKT/mTOR signaling pathway

Zhang

Ren²,

Sun³

et al. 2021

Saudi Journal of Biological Sciences

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Background Osteosarcoma (OS) is the most common malignant bone cancer with more metastasis and increased occurrence in children and teen-agers and being responsible for more number of morbidity and mortality worldwide. Objective The current exploration was planned study the in vitro anticancer actions of dieckol against human OS MG-63 cells via PI3K/AKT/mTOR signaling inhibition. Methodology The cytotoxicity of dieckol was scrutinized by MTT assay. Effects of dieckol on the ROS accumulation, apoptotic cell death, and MMP level in the MG-63 cells were studied by respective fluorescence staining assays. The levels of proliferative, inflammatory, and apoptotic markers in the dieckol treated MG-63 cells were scrutinized by marker specific kits. The expressions of PI3K, AKT, and mTOR was assayed by RT-PCR. Results The MTT assay revealed that the dieckol dose dependently prevented MG-63 cells viability and the IC50 was found at 15 µM. Dieckol treatment effectively reduced the MMP level and improved the ROS generation and apoptosis in MG-63 cells. Dieckol also regulated the proliferative (cyclin D1), inflammatory (COX-2, IL-6, TNF-α, and NF-κB), and apoptotic (caspase-3, Bax, Bcl-2) markers in the MG-63 cells. The PI3K/AKT/mTOR signaling in the MG-63 cells were effectively inhibited by the dieckol treatment. Conclusion In conclusion, our findings from this study recommends that the dieckol could be a talented anticancer candidate for the OS management in the future.

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Section: Discussionmentioning

confidence: 99%

Dieckol exerts anticancer activity in human osteosarcoma (MG-63) cells through the inhibition of PI3K/AKT/mTOR signaling pathway

Zhang

Ren²,

Sun³

et al. 2021

Saudi Journal of Biological Sciences

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“…15 By contrast, SC suppressed osteosarcoma cell proliferation and stimulated cell cycle arrest by impairing the PI3K/AKT activation. 25 In the same vein, we noted that SC reduced the extents of PI3K and AKT phosphorylation in parental and DDP-resistant CC cells, which was partially restored by PTPN1 overexpression. To further substantiate the involvement of the PI3K/AKT pathway deficit in SCmediated DDP chemosensitivity, we delivered the PI3K/ AKT pathway agonist Recilisib into CC cells treated with DDP and SC.…”

Section: Discussionmentioning

confidence: 60%

Combination of Sodium Cantharidinate with Cisplatin Synergistically Hampers Growth of Cervical Cancer

Xiangxun¹,

Zhou²,

Fan³

et al. 2021

DDDT

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“…The PI3K/AKT signaling pathway stabilized Cyclin D1 and promotes Cyclin D1 expression (D'Amico et al, 2000). Sodium cantharidinate suppressed human osteosarcoma MG‐63 cell proliferation and induced cell cycle arrest at the G0/G1 phase, decreased Cyclin D1 and CDK6 expression via inhibition of the PI3K/AKT signaling pathway (Kong, Liu, Wang, Liu, & Zhang, 2019). Oxymatrine inhibited cell proliferation, arrested cell cycle at the G0/G1 phase, and decreased Cyclin D1 and CDK6 expression via inhibition of the PI3K/Akt/mTOR signaling pathway in human glioblastoma cells (Dai et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

ERO1α promotes testosterone secretion in hCG‐stimulated mouse Leydig cells via activation of the PI3K/AKT/mTOR signaling pathway

Chen

Wang

Liu

et al. 2020

Journal Cellular Physiology

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ER oxidoreduclin 1α (ERO1α) is an oxidase, participating in formation of secretory and membrane proteins. However, the other physiological functions ERO1α is not well known. We found that ERO1α is high in the Leydig cells of the testis. Therefore, the purposes of the current study are to explore the role of ERO1α and the possible mechanisms in regulating cell proliferation, apoptosis, and testosterone secretion of Leydig cells. ERO1α was mainly localized in Leydig cells in the adult mice testes by immunofluorescence staining. Western blot analysis showed that ERO1α was higher in Leydig cells than that in the seminiferous tubules. The effect of ERO1α on cell proliferation, apoptosis, and testosterone secretion was detected by transducing ERO1α overexpression and knockdown lentiviruses into cultured primary Leydig cells (PLCs) together with hCG exposure. Flow cytometry analysis showed that ERO1α promoted cell proliferation by increasing cell distribution at the S phase and decreasing that at the G0/G1 phase. Western bolt analysis showed that ERO1α increased CDK2 and CDK6 expression. Cell apoptosis determination found that ERO1α inhibited PLC apoptosis. Western bolt analysis showed that ERO1α increased the ratio of BCL‐2/BAX, and decreased BAD and Caspase‐3 expression. Enzyme‐linked immunosorbent assay analysis demonstrated that ERO1α enhanced testosterone secretion. Western bolt analysis found that ERO1α increased StAR, 3β‐HSD, and CYP17A1 expression. Furthermore, ERO1α could activate the PI3K/AKT/mTOR signaling pathway. In summary, these results suggest that ERO1α might play proliferation promotion and antiapoptotic roles and enhance testosterone secretion in PLC, at least partly, via activation of the PI3K/AKT/mTOR signaling pathway.

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Sodium cantharidinate suppresses human osteosarcoma MG‑63 cell proliferation and induces cell cycle arrest by inhibition of PI3K/AKT activation

Cited by 6 publications

References 24 publications

Dieckol exerts anticancer activity in human osteosarcoma (MG-63) cells through the inhibition of PI3K/AKT/mTOR signaling pathway

Dieckol exerts anticancer activity in human osteosarcoma (MG-63) cells through the inhibition of PI3K/AKT/mTOR signaling pathway

Combination of Sodium Cantharidinate with Cisplatin Synergistically Hampers Growth of Cervical Cancer

ERO1α promotes testosterone secretion in hCG‐stimulated mouse Leydig cells via activation of the PI3K/AKT/mTOR signaling pathway

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