Epigenetic regulation of autophagy in gastrointestinal cancers

Ghavami, Saeid; Zamani, Mozhdeh; Ahmadi, Mazaher; Erfani, Mehran; Dastghaib, Sanaz; Darbandi, Mahsa; Darbandi, Sara; Vakili, Omid; Siri, Morvarid; Grabarek, Beniamin Oskar; Boroń, Dariusz; Zarghooni, Maryam; Wiecheć, Emilia; Mokarram, Pooneh

doi:10.1016/j.bbadis.2022.166512

Cited by 28 publications

(12 citation statements)

References 256 publications

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“…Autophagy not only leads to the elimination of misfolded proteins and damaged organelles, it also modulates the recycling of components within the cell thereby ensuring the cellular quality control (130)(131)(132). The primary function of autophagy is survival under stress conditions, such as starvation (133). This is accomplished through self-eating that provides the cell with required energy and metabolic precursors (134)(135)(136)(137).…”

Section: Role Of Cers and Ceramides In Regulation Of Autophagymentioning

confidence: 99%

Ceramides and Ceramide Synthases in Cancer: Focus on Apoptosis and Autophagy

Alizadeh¹,

Rosa²,

Weng³

et al. 2023

Preprint

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Different studies corroborate a role for ceramide synthases and their downstream products, ceramides, in modulation of apoptosis and autophagy in the context of cancer. These mechanisms of regulation, however, appear to be context dependent in terms of ceramides’ fatty acid chain length, subcellular localization, and the presence or absence of their downstream targets. Our current understanding of the role of ceramide synthases and ceramides in regulation of apoptosis and autophagy could be harnessed to pioneer the development of new treatments to activate or inhibit a single type of ceramide synthase, thereby regulating the apoptosis induction or cross talk of apoptosis and autophagy in cancer cells. Moreover, the apoptotic function of ceramide suggests that ceramide analogues can pave the way for the development of novel cancer treatments. Therefore, in the current review paper we discuss the impact of ceramide synthases and ceramides in regulation of apoptosis and autophagy in context of different types of cancers. We also briefly introduce the latest methods to analyze the lipids in biological samples. Finally, we discuss the drug development strategies focusing on the ceramide synthases and ceramides as future therapeutic approaches in cancer therapy.

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Section: Role Of Cers and Ceramides In Regulation Of Autophagymentioning

confidence: 99%

Ceramides and Ceramide Synthases in Cancer: Focus on Apoptosis and Autophagy

Alizadeh¹,

Rosa²,

Weng³

et al. 2023

Preprint

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“…The autophagosomes then fuse with lysosomes, which contain hydrolases, resulting in the degradation and recycling of cargo contents [9][10][11]. Microautophagy is the direct fusion of cargo with lysosomes.…”

Section: Introductionmentioning

confidence: 99%

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

Alizadeh¹,

Kavoosi²,

Singh³

et al. 2023

Preprint

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Metabolic changes are an important component of tumor cell progression. Tumor cells adapt to environmental stresses via changes to carbohydrate and lipid metabolism. Autophagy, a physiological process in mammalian cells that digests damaged organelles and misfolded proteins via lysosomal degradation is closely associated with metabolism in mammalian cells acting as a meter of cellular ATP levels. In this review, we discuss the changes in glycolytic and lipid biosynthetic pathways in mammalian cells and their impact on carcinogenesis via the autophagy pathway. Also, we discuss the impact of these metabolic pathways on autophagy in lung cancer.

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“…For example, Zhao et al ( 26 ) determined that the lncRNA CRNDE is capable of inducing autophagy in glioblastoma, thereby reducing tumor cell sensitivity to chemotherapeutic treatment. Epigenetic alterations can modify several genes and modulators, eventually leading to inhibition or promotion of autophagy in different cancer stages, and mediating chemoresistance or chemosensitivity ( 27 ). Also, lncRNA KCNQ1OT1 reduced small cell lung cancer (SCLC) tumor growth and chemoresistance via the JAK2/STAT3 signaling pathway ( 28 ).…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG7 promotes non-small cell lung cancer progression and cisplatin resistance by inducing autophagic activity

She¹,

He²,

Xiao³

et al. 2023

J Thorac Dis

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Background Cisplatin (DDP) is among the most widely used chemotherapeutic drugs for non-small cell lung cancer (NSCLC), yet the frequent emergence of chemoresistance serves as a major barrier to the treatment of this tumor type. Long non-coding RNAs (lncRNAs) have recently been shown to influence the ability of cells to resist particular chemotherapy drugs. The present study was developed to explore the role of the lncRNA SNHG7 as a regulator of NSCLC cell chemosensitivity. Methods Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to measure SNHG7 expression in NSCLC tissues from patients that were sensitive/resistant to DDP, correlations between SNHG7 expression levels and the patients’ clinicopathological characteristics were assessed, and the prognostic relevance of SNHG7 expression was examined via the Kaplan-Meier approach. In addition, SNHG7 expression was assessed in NSCLC cell lines that were DDP-sensitive or -resistant, while western blotting and immunofluorescence staining were employed to detect autophagy-associated protein expression in A549, A549/DDP, HCC827, and HCC827/DDP cells. NSCLC cell chemoresistance was quantified via the Cell Counting Kit-8 (CCK-8) assay approach, and flow cytometry was used to detect the apoptotic death of these tumor cells. The chemosensitivity of xenograft tumors in vivo was further assessed to validate the functional importance of SNHG7 as a regulator of NSCLC DDP resistance. Results Relative to paracancerous tissues, NSCLC tumors exhibited SNHG7 upregulation, and this lncRNA was further upregulated in DDP-resistant patients compared to chemosensitive patients. Consistently, higher SNHG7 expression levels were correlated with worse patient survival outcomes. DDP-resistant NSCLC cells were also found to exhibit higher levels of SNHG7 expression than chemosensitive cells, and knocking down this lncRNA enhanced the sensitivity of these cells to DDP treatment, resulting in impaired proliferation and higher rates of apoptotic death. Knocking down SNHG7 was also sufficient to suppress microtubule associated protein 1 light chain 3 beta (LC3B) and Beclin1 protein levels and promote p62 upregulation in vitro . The silencing of this lncRNA additionally inhibited the resistance of NSCLC xenograft tumors to DDP treatment in vivo. Conclusions SNHG7 can promote malignant behaviors and DDP resistance in NSCLC cells at least partly via the induction of autophagic activity.

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Epigenetic regulation of autophagy in gastrointestinal cancers

Cited by 28 publications

References 256 publications

Ceramides and Ceramide Synthases in Cancer: Focus on Apoptosis and Autophagy

Ceramides and Ceramide Synthases in Cancer: Focus on Apoptosis and Autophagy

Regulation of Autophagy via Carbohydrate and Lipid Metabolism in Cancer

LncRNA SNHG7 promotes non-small cell lung cancer progression and cisplatin resistance by inducing autophagic activity

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