Autophagy and its role in osteosarcoma

Ning, Biao; Liu, Yixin; Huang, Tianhe; Wei, Yongchang

doi:10.1002/cam4.5407

Cited by 11 publications

(9 citation statements)

References 114 publications

(235 reference statements)

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“…On the other hand, if this process is overactive, cells may excessively degrade and eventually die, including cancer cells ( 45 ). Studies have shown that in breast cancer, osteosarcoma and pancreatic cancer, inducing autophagy can significantly inhibit growth and proliferation ( 46 – 48 ). The present results also showed that rapamycin induced B16 melanoma cell autophagy and suppressed cell viability in a dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Rapamycin inhibits B16 melanoma cell viability in vitro and in vivo by inducing autophagy and inhibiting the mTOR/p70‑S6k pathway

Wang,

Zhang,

Guo

et al. 2024

Oncol Lett

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Rapamycin is an immunosuppressant that has been shown to prevent tumor growth following organ transplantation. However, its exact mode of antitumor action remains unknown. The present study used the B16-F10 (B16) murine melanoma model to explore the antitumor mechanism of rapamycin, and it was revealed that rapamycin reduced B16 cell viability in vitro and in vivo . In addition, in vitro and in vivo , the results of western blotting showed that rapamycin reduced Bcl2 expression, and enhanced the protein expression levels of cleaved caspase 3 and Bax, indicating that it can induce the apoptosis of B16 melanoma cells. Furthermore, the results of cell cycle analysis and western blotting showed that rapamycin induced B16 cell cycle arrest in the G 1 phase, based on the reduction in the protein expression levels of CDK1, cyclin D1 and CDK4, as well as the increase in the percentage of cells in G 1 phase. Rapamycin also significantly increased the number of autophagosomes in B16 melanoma cells, as determined by transmission electron microscopy. Furthermore, the results of RT-qPCR and western blotting showed that rapamycin upregulated the protein expression levels of microtubule-associated protein light chain 3 (LC3) and Beclin-1, while downregulating the expression of p62 in vitro and in vivo , thus indicating that rapamycin could trigger cellular autophagy. The present study revealed that rapamycin in combination with chloroquine (CQ) further increased LC3 expression compared with that in the CQ group, suggesting that rapamycin induced an increase in autophagy in B16 cells. Furthermore, the results of western blotting showed that rapamycin blocked the phosphorylation of p70 ribosomal S6 kinase (p70-S6k) and mammalian target of rapamycin (mTOR) proteins in vitro and in vivo , thus suggesting that rapamycin may exert its antitumor effect by inhibiting the phosphorylation of the mTOR/p70-S6k pathway. In conclusion, rapamycin may inhibit tumor growth by inducing cellular G 1 phase arrest and apoptosis. In addition, rapamycin may exert its antitumor effects by inducing the autophagy of B16 melanoma cells in vitro and in vivo , and the mTOR/p70-S6k signaling pathway may be involved in this process.

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Section: Discussionmentioning

confidence: 99%

Rapamycin inhibits B16 melanoma cell viability in vitro and in vivo by inducing autophagy and inhibiting the mTOR/p70‑S6k pathway

Wang,

Zhang,

Guo

et al. 2024

Oncol Lett

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“…In addition, autophagy also has dual role to osteosarcoma; it can both promote and inhibit the development of osteosarcoma depending on different mechanism. 25 , 26 , 27 , 28 Necroptosis is induced by TNFR1/RIP1, 3/MLKL signal pathway, which damage cell structure. 29 The long noncoding RNA (lncRNA) has been proved to have high connection with osteosarcoma.…”

Section: Introductionmentioning

confidence: 99%

The role of programmed cell death in osteosarcoma: From pathogenesis to therapy

Liu,

Wang

et al. 2024

Cancer Medicine

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Osteosarcoma (OS) is a prevalent bone solid malignancy that primarily affects adolescents, particularly boys aged 14–19. This aggressive form of cancer often leads to deadly lung cancer due to its high migration ability. Experimental evidence suggests that programmed cell death (PCD) plays a crucial role in the development of osteosarcoma. Various forms of PCD, including apoptosis, ferroptosis, autophagy, necroptosis, and pyroptosis, contribute significantly to the progression of osteosarcoma. Additionally, different signaling pathways such as STAT3/c‐Myc signal pathway, JNK signl pathway, PI3k/AKT/mTOR signal pathway, WNT/β‐catenin signal pathway, and RhoA signal pathway can influence the development of osteosarcoma by regulating PCD in osteosarcoma cell. Therefore, targeting PCD and the associated signaling pathways could offer a promising therapeutic approach for treating osteosarcoma.

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“…As there has been no significant increase in the survival rate of patients with metastatic disease over recent decades ( Ning et al, 2023 ), numerous studies have focused on understanding the molecular mechanisms underlying tumorigenesis and drug resistance in osteosarcoma. Targeted therapy, which includes immune system targets, drug delivery systems, as well as intercellular and extracellular signaling pathways of metabolism, has advanced rapidly in recent years ( Shaikh et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Therapeutic potential of tyrosine-protein kinase MET in osteosarcoma

Zeng,

Liu,

Gong

et al. 2024

Front. Mol. Biosci.

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Osteosarcoma, the most prevalent primary bone tumor in children and young adults, can often be successfully treated with standard chemotherapy and surgery when diagnosed at an early stage. However, patients presenting with metastases face significant challenges in achieving a cure. Despite advancements in classical therapies over the past few decades, clinical outcomes for osteosarcoma have not substantially improved. Recently, there has been increased understanding of the biology of osteosarcoma, leading to the identification of new therapeutic targets. One such target is MET, a tyrosine kinase receptor for Hepatocyte Growth Factor (HGF) encoded by the MET gene. In vitro and in vivo studies have demonstrated that the HGF/MET pathway plays a crucial role in cancer growth, invasion, metastasis, and drug resistance across various cancers. Clinical trials targeting this pathway are already underway for lung cancer and hepatocellular carcinoma. Moreover, MET has also been implicated in promoting osteosarcoma progression. This review summarizes 3 decades’ worth of research on MET’s involvement in osteosarcoma and further explores its potential as a therapeutic target for patients with this disease.

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Autophagy and its role in osteosarcoma

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 11 publications

References 114 publications

Rapamycin inhibits B16 melanoma cell viability in vitro and in vivo by inducing autophagy and inhibiting the mTOR/p70‑S6k pathway

Rapamycin inhibits B16 melanoma cell viability in vitro and in vivo by inducing autophagy and inhibiting the mTOR/p70‑S6k pathway

The role of programmed cell death in osteosarcoma: From pathogenesis to therapy

Therapeutic potential of tyrosine-protein kinase MET in osteosarcoma

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