Inhibition of autophagy and enhancement of endoplasmic reticulum stress increase sensitivity of osteosarcoma Saos‐2 cells to cannabinoid receptor agonist WIN55,212‐2

Zhang, Guodong; Bi, Hong‐Yan; Gao, Ji; Lü, Xing; Zheng, Yanping

doi:10.1002/cbf.3194

Cited by 10 publications

(3 citation statements)

References 29 publications

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“…Cannabinoid‐induced death signaling can also target intracellular organelles such as mitochondria or endoplasmatic reticulum (ER), as well as essential, substantially protective cellular functions such as autophagy. These in turn can become overactivated, resulting in cell death in various types of cancer cells in culture . Changes in the expression pattern of stress‐regulated transcriptional regulators that are involved in tumorigenesis as well as tumor progression might also be contributors to cannabinoid‐mediated cell death .…”

Section: The Cannabinoid System As a Target In Cancermentioning

confidence: 99%

Synergistic interaction of the cannabinoid and death receptor systems – a potential target for future cancer therapies?

Keresztes

Streicher

2017

FEBS Letters

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Edited by Lukas Alfons HuberCannabinoid receptors have been shown to interact with other receptors, including tumor necrosis factor receptor superfamily (TNFRS) members, to induce cancer cell death. When cannabinoids and death-inducing ligands (including TNF-related apoptosis-inducing ligand) are administered together, they have been shown to synergize and demonstrate enhanced antitumor activity in vitro. Certain cannabinoid ligands have been shown to sensitize cancer cells and synergistically interact with members of the TNFRS, thus suggesting that the combination of cannabinoids with death receptor (DR) ligands induces additive or synergistic tumor cell death. This review summarizes recent findings on the interaction of the cannabinoid and DR systems and suggests possible clinical co-application of cannabinoids and DR ligands in the treatment of various malignancies.

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Section: The Cannabinoid System As a Target In Cancermentioning

confidence: 99%

Synergistic interaction of the cannabinoid and death receptor systems – a potential target for future cancer therapies?

Keresztes

Streicher

2017

FEBS Letters

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“…It has been demonstrated to confer radioresistance to BOS cells due to hypoxia induction (44). Prevention of autophagy has been shown to enhance the sensitivity of BOS cell lines to cannabinoid receptor agonist through the induction of apoptosis (45). It has also been shown to enhance type 2 programmed cell death in BOS following induction by some agents (46,47).…”

Section: Role Of Autophagy In Bosmentioning

confidence: 99%

Osteogenic Sarcoma: A 21st Century Review

Osasan

Zhang

Shen

et al. 2016

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“…Cannabinoid therapy promotes cancerous cell death, reduction of tumour angiogenesis, as well as blockade of invasion and metastasis. Cannabinoid anticancer mechanism is substantially related to inducing autophagy mediated apoptotic cancer cell death (21,22). In addition to the cancer cell death, treatment with cannabinoids has been shown to normalize the tumour vasculature, which is considered to be based on the inhibition of the endothelial growth factor (VEGF) pathway.…”

Section: Introductionmentioning

confidence: 99%

Anti-cancer effects of selective cannabinoid agonists in pancreatic and breast cancer cells

Turgut¹,

ARMAGAN²,

KASAPLIGIL³

et al. 2022

BLL

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OBJECTIVE: Cancer ranks fi rst among the causes of morbidity and mortality all over the world, and it is expected to continue to be the main cause of death in the coming years. Therefore, new molecular targets and therapeutic strategies are urgently needed. In many cases, some reports show increased levels of endocannabinoids and their receptors in cancer, a condition often associated with tumour aggressiveness. Recent studies have suggested that cannabinoid-1/2 receptors contribute to tumour growth in a variety of cancers, including pancreatic, colon, prostate, and breast cancer. Understanding how cannabinoids can regulate key cellular processes involved in tumorigenesis, such as: cell proliferation and cell death, is crucial to improving existing and new therapeutic approaches for the cancer patients. The present study was aimed to characterize the in-vitro effect of L-759633 (a selective CB2 receptor agonist), ACPA (a selective CB1 receptor agonist) and ACEA (a selective CB1 receptor agonist) on the cell proliferation, clonogenicity, and apoptosis in pancreatic (PANC1) and breast (MDA-MB-231) cancer cells. METHODS: The viability and/or proliferation of cells were detected by MTS assay. A clonogenic survival assay was used to detect the ability of a single cell to grow into a colony. Apoptosis was determined with Annexin V staining (Annexin V-FITC/PI test) and by analyzing the expression of Bcl-2-associated X protein (Bax) and B-cell lymphoma 2 (Bcl-2). RESULTS: We found that selective CB1/2 agonists suppressed cell proliferation, clonogenicity and induced proapoptotic function in human PANC1 pancreatic and MDA-MB-231 breast cancer cells. Based on our fi ndings, these agonists led to the inhibition of both cell viability and clonogenic growth in a dose dependent manner. CB1/2 agonists were observed to induce intrinsic apoptotic pathway by upregulating Bax, while downregulating Bcl-2 expression levels. CONCLUSION: Our data suggests that CB1/2 agonists have the therapeutic potential through the inhibition of survival of human PANC1 pancreatic and MDA-MB-231 breast cancer cells and also might be linked with further cellular mechanisms for the prevention (Fig. 5, Ref. 49).

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Inhibition of autophagy and enhancement of endoplasmic reticulum stress increase sensitivity of osteosarcoma Saos‐2 cells to cannabinoid receptor agonist WIN55,212‐2

Cited by 10 publications

References 29 publications

Synergistic interaction of the cannabinoid and death receptor systems – a potential target for future cancer therapies?

Synergistic interaction of the cannabinoid and death receptor systems – a potential target for future cancer therapies?

Osteogenic Sarcoma: A 21st Century Review

Anti-cancer effects of selective cannabinoid agonists in pancreatic and breast cancer cells

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