FasL on the surface of Tag7 (PGRP-S)-activated lymphocytes induces necroptosis in HLA-negative tumor cells with the involvement of lysosomes and mitochondria

Sharapova, Tatiana N.; Романова, Е. А.; Sashchenko, Lidia P.; Yashin, Denis V.

doi:10.1016/j.biochi.2018.07.003

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…As shown in Figures 5A-C, the anti-tumor effects of PD were reduced after the expression of FOXO3a was suppressed in vivo. Bim, Fasl and TRAIL are downstream genes of FOXO3a (31)(32)(33)46). PD increased the protein expression levels of all three of these in PC3 cells (Figure 5D).…”

Section: Pd Regulates the Downstream Targets Of Foxo3amentioning

confidence: 91%

“…Docetaxel has been shown to induce cancer cell apoptosis at least partly by enhancing FOXO3a activity and stimulating its nuclear translocation (30). The overexpression of FOXO-responsive genes, such as Bim (31), FasL (32) and TRAIL (33), leads to the induction of cell death. However, the response of FOXO3a to sorafenib exposure in prostate cancer cells is unclear.…”

Section: Introductionmentioning

confidence: 99%

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Combined Anti-Cancer Effects of Platycodin D and Sorafenib on Androgen-Independent and PTEN-Deficient Prostate Cancer

Song

Zhang

et al. 2021

Front. Oncol.

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Castration-resistant (androgen-independent) and PTEN-deficient prostate cancer is a challenge in clinical practice. Sorafenib has been recommended for the treatment of this type of cancer, but is associated with several adverse effects. Platycodin D (PD) is a triterpene saponin with demonstrated anti-cancer effects and a good safety profile. Previous studies have indicated that PC3 cells (PTEN -/-, AR -/-) are sensitive to PD, suggesting that it may also be a useful treatment for castration-resistance prostate cancer. We herein investigated the effects of combining PD with sorafenib to treat PTEN-deficient prostate cancer cells. Our data show that PD promotes sorafenib-induced apoptosis and cell cycle arrest in PC3 cells. Of interest, PD only promoted the anti-cancer effects of sorafenib in Akt-positive and PTEN-negative prostate cancer cells. Mechanistic studies revealed that PD promoted p-Akt ubiquitination by increasing the p-Akt level. PD also increased the protein and mRNA expression of FOXO3a, the downstream target of Akt. Meanwhile, PD promoted the activity of FOXO3a and increased the protein expression of Fasl, Bim and TRAIL. Interestingly, when FOXO3a expression was inhibited, the antitumor effects of both PD and sorafenib were individually inhibited, and the more potent effects of the combination treatment were inhibited. Thus, the combination of PD and sorafenib may exert potent anti-cancer effects specifically via FOXO3a. The use of Akt inhibitors or FOXO3a agonists, such as PD, may represent a promising approach for the treatment of androgen-independent and PTEN-deficient prostate cancer.

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Section: Pd Regulates the Downstream Targets Of Foxo3amentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Combined Anti-Cancer Effects of Platycodin D and Sorafenib on Androgen-Independent and PTEN-Deficient Prostate Cancer

Song

Zhang

et al. 2021

Front. Oncol.

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“…Necroptosis is another type of regulated cell death closely related to the receptor-interacting protein kinases 1 and 3 (RIPK1 and RIPK3) and mixed-lineage kinase domain-like protein (MLKL) [ 107 ]. Necroptosis begins with the activation of RIPK and MLKL, which increase the levels of Ca 2+ , causing lysosomal membrane permeabilization, and release cathepsins into the cytosol [ 108 ]. Although relevant studies are scarce, a recent report has shown that inducing necroptosis in cancer cells can overcome chemotherapy failure due to apoptotic resistance [ 109 ], while metal complexes have been shown to induce cancer cell death through necroptosis [ 110 , 111 ].…”

Section: Ru(ii) Complexesmentioning

confidence: 99%

Ruthenium Complexes as Promising Candidates against Lung Cancer

Sun

Shi

et al. 2021

Molecules

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Lung cancer is one of the most common malignancies with the highest mortality rate and the second-highest incidence rate after breast cancer, posing a serious threat to human health. The accidental discovery of the antitumor properties of cisplatin in the early 1960s aroused a growing interest in metal-based compounds for cancer treatment. However, the clinical application of cisplatin is limited by serious side effects and drug resistance. Therefore, other transition metal complexes have been developed for the treatment of different malignant cancers. Among them, Ru(II/III)-based complexes have emerged as promising anticancer drug candidates due to their potential anticancer properties and selective cytotoxic activity. In this review, we summarized the latest developments of Ru(II/III) complexes against lung cancer, focusing mainly on the mechanisms of their biological activities, including induction of apoptosis, necroptosis, autophagy, cell cycle arrest, inhibition of cell proliferation, and invasion and metastasis of lung cancer cells.

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“…However, it is still unclear how acinar cell necrosis is initiated and what kind of factors are involved in the earlier stages of AP. It is known that the initiation of necroptosis can be triggered by different endogenous and exogenous factors, such as TNF‐α, factor‐associated suicide ligand, TNF‐related apoptosis‐inducing ligand, reactive oxygen species, activated Toll‐like receptors (TLRs), type I interferons and certain pathogens 33,34 . However, the endogenous trigger of acinar cell necroptosis during AP has not yet been fully addressed.…”

Section: Discussionmentioning

confidence: 99%

Serum amyloid A3 is required for caerulein‐induced acute pancreatitis through induction of RIP3‐dependent necroptosis

Yang

et al. 2020

Immunol Cell Biol

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Serum amyloid A (SAA) is an early and sensitive biomarker of inflammatory diseases, but its role in acute pancreatitis (AP) is still unclear. Here, we used a caerulein‐induced mouse model to investigate the role of SAA in AP and other related inflammatory responses. In our study, we found that the expression of a specific SAA isoform, SAA3, was significantly elevated in a caerulein‐induced AP animal model. In addition, SAA3‐knockout (Saa3−/−) mice showed lower serum levels of amylase and lipase, tissue damage and proinflammatory cytokine production in the pancreas compared with those of wild‐type mice in response to caerulein administration. AP‐associated acute lung injury was also significantly attenuated in Saa3−/− mice. In our in vitro experiments, treatment with cholecystokinin and recombinant SAA3 significantly induced necroptosis and cytokine production. Moreover, we found that the regulatory effect of SAA3 on acinar cell necroptosis was through a receptor‐interacting protein 3 (RIP3)‐dependent manner. Collectively, our findings indicate that SAA3 is required for AP by inducing an RIP3‐dependent necroptosis pathway in acinar cells and is a potential drug target for AP.

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FasL on the surface of Tag7 (PGRP-S)-activated lymphocytes induces necroptosis in HLA-negative tumor cells with the involvement of lysosomes and mitochondria

Cited by 18 publications

References 38 publications

Combined Anti-Cancer Effects of Platycodin D and Sorafenib on Androgen-Independent and PTEN-Deficient Prostate Cancer

Combined Anti-Cancer Effects of Platycodin D and Sorafenib on Androgen-Independent and PTEN-Deficient Prostate Cancer

Ruthenium Complexes as Promising Candidates against Lung Cancer

Serum amyloid A3 is required for caerulein‐induced acute pancreatitis through induction of RIP3‐dependent necroptosis

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