MYC is a positive regulator of choline metabolism and impedes mitophagy-dependent necroptosis in diffuse large B-cell lymphoma

Xiong, Jie; Wang, L; Xc, Fei; Xf, Jiang; Zheng, Zhi; Zhao, Yingying; Cf, Wang; B, Li; Sj, Chen; Janin, Anne; Rp, Gale; Wl, Zhao

doi:10.1038/bcj.2017.61

Cited by 45 publications

(48 citation statements)

References 42 publications

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“…Besides coordinating with HIF-1α the expression of several glucose transporters and glycolytic enzymes [213,214], c-Myc also modulates mitophagy by regulating choline metabolism. In B-lymphoma cells, c-Myc activates the transcription of the key enzyme phosphate cytidylyltransferase 1 choline-α (PCYT1A) and PCYT1A upregulation prevents lymphoma cells to undergo a mitophagy-dependent necroptosis [215].…”

Section: Mitophagy and Cancermentioning

confidence: 99%

Mitophagy in Cancer: A Tale of Adaptation

Vara-Pérez

Felipe‐Abrio

Agostinis

2019

Cells

180

134

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In the past years, we have learnt that tumors co-evolve with their microenvironment, and that the active interaction between cancer cells and stromal cells plays a pivotal role in cancer initiation, progression and treatment response. Among the players involved, the pathways regulating mitochondrial functions have been shown to be crucial for both cancer and stromal cells. This is perhaps not surprising, considering that mitochondria in both cancerous and non-cancerous cells are decisive for vital metabolic and bioenergetic functions and to elicit cell death. The central part played by mitochondria also implies the existence of stringent mitochondrial quality control mechanisms, where a specialized autophagy pathway (mitophagy) ensures the selective removal of damaged or dysfunctional mitochondria. Although the molecular underpinnings of mitophagy regulation in mammalian cells remain incomplete, it is becoming clear that mitophagy pathways are intricately linked to the metabolic rewiring of cancer cells to support the high bioenergetic demand of the tumor. In this review, after a brief introduction of the main mitophagy regulators operating in mammalian cells, we discuss emerging cell autonomous roles of mitochondria quality control in cancer onset and progression. We also discuss the relevance of mitophagy in the cellular crosstalk with the tumor microenvironment and in anti-cancer therapy responses.

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Section: Mitophagy and Cancermentioning

confidence: 99%

Mitophagy in Cancer: A Tale of Adaptation

Vara-Pérez

Felipe‐Abrio

Agostinis

2019

Cells

180

134

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“…Besides its widely documented apoptotic anticancer activity [ 163 ], berberine promoted necroptosis in ovarian cancer cells and in three patient-derived primary ovarian cancer cell lines (POCCLs) by activating RIP3 and MLKL [ 118 ] ( Table 2 ). Berberine triggered necroptosis also in diffuse large B-cell lymphoma (DLBCL) cancer cells, where the necroptotic mechanism has been deeply investigated [ 119 ] ( Table 2 ). In DLBCL cells, berberine promoted mitophagy-dependent necroptosis by inducing the formation of the RIP1/RIP3/MLKL necrosome complex and mRNA degradation of PCYT1A (phosphate cytidylyltransferase 1 alpha), thus reducing its expression in cancer cells [ 119 ] ( Table 2 ).…”

Section: Necroptosismentioning

confidence: 99%

Natural Products as Inducers of Non-Canonical Cell Death: A Weapon against Cancer

Greco

Catanzaro

Fimognari

2021

Cancers

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Apoptosis has been considered the main mechanism induced by cancer chemotherapeutic drugs for a long time. This paradigm is currently evolving and changing, as increasing evidence pointed out that antitumor agents could trigger various non-canonical or non-apoptotic cell death types. A considerable number of antitumor drugs derive from natural sources, both in their naturally occurring form or as synthetic derivatives. Therefore, it is not surprising that several natural compounds have been explored for their ability to induce non-canonical cell death. The aim of this review is to highlight the potential antitumor effects of natural products as ferroptosis, necroptosis, or pyroptosis inducers. Natural products have proven to be promising non-canonical cell death inducers, capable of overcoming cancer cells resistance to apoptosis. However, as discussed in this review, they often lack a full characterization of their antitumor activity together with an in-depth investigation of their toxicological profile.

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“…PCYT1A is a rate-limiting enzyme for PC synthesized via the Kennedy pathway, which converts phosphocholine to CDP-choline 31 . Many studies have reported that the increase of PC synthesis is caused by the up-regulation of PCYT1A 11,19,31,32 . Furthermore, we examined the levels of the substrates for the PC biosynthesis in HepG2 and HepG2.2.15 cells and found that phosphocholine and CDP-choline increased in HepG2.2.15 cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Stimulated phospholipid synthesis is key for hepatitis B virus replications

Huang

Lei

Ding

et al. 2019

Sci Rep

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Chronic hepatitis B Virus (HBV) infection has high morbidity, high pathogenicity and unclear pathogenesis. To elucidate the relationship between HBV replication and host phospholipid metabolites, we measured 10 classes of phospholipids in serum of HBV infected patients and cells using ultra performance liquid chromatograph-triple quadruple mass spectrometry. We found that the levels of phosphatidylcholine (PC), phosphatidylethanolamine, and lyso-phosphatidic acid were increased in HBsAg (+) serum of infected patients compared with HBsAg (−), while phosphatidylserine, phosphatidylglycerol, phosphatidylinositol, and sphingomyelin were decreased, which were confirmed in an HBV infected HepG2.2.15 cell line. We further evaluated the enzyme levels of PC pathways and found that PCYT1A and LPP1 for PC synthesis were up-regulated after HBV infection. Moreover, HBV replication was inhibited when PCYT1A and LPP1 were inhibited. These results indicated that the PC synthesis in HBV infected host are regulated by PCYT1A and LPP1, which suggests that PCYT1A, LPP1 could be new potential targets for HBV treatment.

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MYC is a positive regulator of choline metabolism and impedes mitophagy-dependent necroptosis in diffuse large B-cell lymphoma

Cited by 45 publications

References 42 publications

Mitophagy in Cancer: A Tale of Adaptation

Mitophagy in Cancer: A Tale of Adaptation

Natural Products as Inducers of Non-Canonical Cell Death: A Weapon against Cancer

Stimulated phospholipid synthesis is key for hepatitis B virus replications

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