Autophagy in Osteosarcoma

Nehme, Grace; Gordon, Nancy

doi:10.1007/978-3-030-43085-6_11

Cited by 9 publications

(8 citation statements)

References 56 publications

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“…The latest research made clear that oxidative stress and autophagy emerged as important mechanism targets of OS. Moreover, accumulating evidence indicated that activation of oxidative stress and autophagy could inhibit OS progression [21,23]. lncRNA regulates the progression of cells in a variety of ways which includes oxidative stress and autophagy.…”

Section: Discussionmentioning

confidence: 99%

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Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway

Xie

Chang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Allicin, an organic sulfur compound extracted from the bulb of Allium sativum, can potentially prevent various tumors. Our previous study found that allicin can effectively suppress the proliferation of osteosarcoma cells. However, the molecular mechanisms have not been illustrated. In this study, Saos-2 and U2OS osteosarcoma cells were used to investigate the underlying mechanisms. A series of experiments were carried out to authenticate the anticancer property of allicin. Knockdown of lncRNA MALAT1 inhibited the proliferation, invasion and migration and promoted apoptosis of osteosarcoma cells. Knockdown of miR-376a increased the proliferation, invasion, and migration and dropped apoptosis of osteosarcoma cells. Furthermore, knockdown of miR-376a reversed the influences of MALAT1 silencing in osteosarcoma cells. Based on our data, MALAT1 could downregulate the expression of miR-376a, subsequently accelerating osteosarcoma. Moreover, oxidative stress and autophagy were identified as the potential key pathway of allicin. Allicin inhibited osteosarcoma growth and promoted oxidative stress and autophagy via MALATI-miR-376a. We also found that allicin promotes oxidative stress and autophagy to inhibit osteosarcoma growth by inhibiting the Wnt/β-catenin pathway in vivo and in vitro. All data showed that allicin promotes oxidative stress and autophagy of osteosarcoma via the MALATI-miR-376a-Wnt/β-catenin pathway.

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Section: Discussionmentioning

confidence: 99%

“…It carried a big weight in maintaining the metabolic requirements of cells and the renewal of some organelles. In OS, autophagy seems deregulated and could act as an antitumoral process [23]. Allicin can activate autophagy to alleviate the malignant development of thyroid cancer [24] and non-small-cell lung cancer [15].…”

Section: Introductionmentioning

confidence: 99%

Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway

Xie

Chang

Wang

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…However, excessive autophagy can also cause excessive degradation of cytoplasm and organelles, leading to cell death [ 22 ]. Increasing evidence in the literature indicated that autophagy played multiple roles in the occurrence, metastasis and chemotherapy resistance of osteosarcoma [ 15 , 23 , 24 ]. Therefore, we constructed an ARGs-based prognostic risk model in our study, which will provide new insights into individualized therapy strategies for osteosarcoma patients.…”

Section: Discussionmentioning

confidence: 99%

Construction and validation of a prognostic model for osteosarcoma patients based on autophagy-related genes

Ning

Liu

et al. 2022

Discov Onc

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Background Osteosarcoma is the most frequent primary bone malignancy with a poor prognosis because of pulmonary metastasis. Autophagy is strongly associated with tumor metastasis, and it is valuable to construct an autophagy-related gene risk model for predicting the prognosis of osteosarcoma. Methods We obtained ARGs from the Human Autophagy Database and RNA-sequencing data of osteosarcoma patients from the Gene Expression Omnibus (GEO) database. Subsequently, univariate and multivariate cox regression analyses were performed to construct a three-gene prognostic model and its accuracy was further confirmed in the Therapeutic Applications Research to Generate Effective Treatments (TARGET) database. Afterward, we detected the expression levels and effects on osteosarcoma cells metastasis of MYC and MBTPS2, which were involved in the model. Results In both training and verification cohorts, patients with lower risk scores had longer OS, and the model was identified as an independent prognostic factor in osteosarcoma. Besides, the ROC curve demonstrated the reliability of the model. Furthermore, RT-qPCR, Western Blotting and IHC results indicated that MYC and MBTPS2 were differently expressed in osteosarcoma tissues and cell lines. MYC knockdown or MBTPS2 overexpression prevented the capacity of migration and invasion in osteosarcoma cell lines through inhibiting cellular autophagy. Conclusion The risk model based on three ARGs had a strong ability to predict the prognosis of osteosarcoma patients. Our findings also suggested that MYC and MBTPS2 were two major factors regulating autophagy in osteosarcoma, and could serve as potential therapeutic targets for osteosarcoma.

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“…For instance, the ATG4B chemical inhibitor (a cysteine proteinase that activates LC3 which is crucial for OS development) may result in autophagy deficiency and a decreased proliferation in vitro and tumor growth in vivo ( 45 ). This indicates that autophagy is capable in promoting proliferation and resistance to anti-cancer therapy in OS tumor cells ( 46 , 47 ). As a result, tumor cells can survive under conditions of hypoxia or nutrient deficiency via autophagy in advanced stages of tumor development.…”

Section: Mechanisms Of Tme-mediated Chemotherapy Resistance In Osmentioning

confidence: 99%

Effects of microenvironment in osteosarcoma on chemoresistance and the promise of immunotherapy as an osteosarcoma therapeutic modality

Zhang

2022

Front. Immunol.

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Osteosarcoma (OS) is one of the most common primary malignant tumors originating in bones. Its high malignancy typically manifests in lung metastasis leading to high mortality. Although remarkable advances in surgical resection and neoadjuvant chemotherapy have lengthened life expectancy and greatly improved the survival rate among OS patients, no further breakthroughs have been achieved. It is challenging to treat patients with chemoresistant tumors and distant metastases. Recent studies have identified a compelling set of links between hypoxia and chemotherapy failure. Here, we review the evidence supporting the positive effects of hypoxia in the tumor microenvironment (TME). In addition, certain anticancer effects of immune checkpoint inhibitors have been demonstrated in OS preclinical models. Continued long-term observation in clinical trials is required. In the present review, we discuss the mutualistic effects of the TME in OS treatment and summarize the mechanisms of immunotherapy and their interaction with TME when used to treat OS. We also suggest that immunotherapy, a new comprehensive and potential antitumor approach that stimulates an immune response to eliminate tumor cells, may represent an innovative approach for the development of a novel treatment regimen for OS patients.

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Autophagy in Osteosarcoma

Cited by 9 publications

References 56 publications

Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway

Allicin Inhibits Osteosarcoma Growth by Promoting Oxidative Stress and Autophagy via the Inactivation of the lncRNA MALAT1-miR-376a-Wnt/β-Catenin Signaling Pathway

Construction and validation of a prognostic model for osteosarcoma patients based on autophagy-related genes

Effects of microenvironment in osteosarcoma on chemoresistance and the promise of immunotherapy as an osteosarcoma therapeutic modality

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