Effect of cholestasis and NeuroAid treatment on the expression of Bax, Bcl-2, Pgc-1α and Tfam genes involved in apoptosis and mitochondrial biogenesis in the striatum of male rats

Nasehi, Mohammad; Torabinejad, Sepehr; Hashemi, Mehrdad; Vaseghi, Salar; Zarrindast, Mohammad‐Reza

doi:10.1007/s11011-019-00508-y

Cited by 25 publications

(14 citation statements)

References 87 publications

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“…In particular, the knockdown of DEPDC1B resulted in not only a significant upregulation of Caspase3, sTNF-R1, but also downregulation of Bcl-2, CD40, HSP27, IGF-1sR, XIAP, Livin, Survivin in chordoma cells. In addition, apoptosis involves both internal and external pathways, in which the endogenous pathway is mediated by an anti-apoptotic protein Bcl-2 (B-cell lymphoma-2) that integrates death and survival signals [ 30 ]. CD40 interacts with CD40 ligand (CD40L) to regulate apoptosis according to different membrane localization [ 31 ].…”

Section: Discussionmentioning

confidence: 99%

DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5

Wang

Tang

et al. 2021

Cell Death Dis

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Chordoma is a rare bone malignancy with a high rate of local recurrence and distant metastasis. Although DEP domain-containing protein 1B (DEPDC1B) is implicated in a variety of malignancies, its relationship with chordoma is unclear. In this study, the biological role and molecular mechanism of DEPDC1B in chordoma were explored. The function of DEPDC1B in chordoma cells was clarified through loss-of-function assays in vitro and in vivo. Furthermore, molecular mechanism of DEPDC1B in chordoma cells was recognized by RNA sequencing and Co-Immunoprecipitation (Co-IP) assay. The malignant behaviors of DEPDC1B knockdown chordoma cells was significantly inhibited, which was characterized by reduced proliferation, enhanced apoptosis, and hindered migration. Consistently, decreased expression of DEPDC1B suppressed tumor growth in xenograft mice. Mechanically, DEPDC1B affected the ubiquitination of baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) through ubiquitin-conjugating enzyme E2T (UBE2T). Simultaneous downregulation of BIRC5 and DEPDC1B may exacerbate the inhibitory effects of chordoma. Moreover, BIRC5 overexpression reduced the inhibitory effects of DEPDC1B knockdown in chordoma cells. In conclusion, DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5, suggesting that it may be a promising candidate target with potential therapeutic value.

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Section: Discussionmentioning

confidence: 99%

DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5

Wang

Tang

et al. 2021

Cell Death Dis

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“…However, the exact reason for aggravation of cardiomyocyte injury needs to be investigated. Lastly, we examined the role of PGC-1α that is reportedly involved in processes related to apoptosis regulation, such as p53 gene-mediated apoptosis, enhancement of mitochondrial recovery to reduce apoptosis, and regulation of the expression of apoptosis-related molecules [67][68][69]. We found that PGC-1α levels gradually decreased with the increase of hypoxia duration, and this change was not affected by NRF-1 inhibition, indicating that PGC-1α is a transcription factor operating upstream of NRF-1.…”

Section: Discussionmentioning

confidence: 99%

Effects of NRF-1 and PGC-1α Cooperation on HIF-1α and Rat Cardiomyocyte Apoptosis Under Hypoxia

Niu

et al. 2021

Preprint

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Hypoxia is a primary inducer of cardiomyocyte injury, its significant marker being hypoxia-induced cardiomyocyte apoptosis. Nuclear respiratory factor-1 (NRF-1) and hypoxia-inducible factor (HIF)-1α are transcriptional regulatory elements implicated in multiple biological functions, including oxidative stress response. However, their roles in hypoxia-induced cardiomyocyte apoptosis remain unknown. The effect HIF-α, together with NRF-1, exerts on cardiomyocyte apoptosis also remains unclear. We established a myocardial hypoxia model and investigated the effects of these proteins on the proliferation and apoptosis of rat cardiomyocytes (H9C2) under hypoxia. Further, we examined the association between NRF-1 and HIF-1α to improve the current understanding of NRF-1 anti-apoptotic mechanisms. The results showed that NRF-1 and HIF-1α are important anti-apoptotic molecules in H9C2 cells under hypoxia, although their regulatory mechanisms differ. NRF-1 could bind to the promoter region of Hif-1α and negatively regulate its expression. Additionally, HIF-1β exhibited competitive binding with NRF-1 and HIF-1α, demonstrating a synergism between NRF-1 and the peroxisome proliferator-activated receptor-gamma coactivator-1α. These results indicate that cardiomyocytes can regulate different molecular patterns to tolerate hypoxia, providing a novel methodological framework for studying cardiomyocyte apoptosis under hypoxia.

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“…Apoptosis is a highly regulated process that contributes to the control of cell number during development and the maintenance of many adult tissues. 29 The B-cell lymphoma-2 (Bcl-2) protein family contains pro-apoptotic proteins and anti-apoptotic proteins. The anti-apoptotic protein Bcl2 is localized on the outer membrane of mitochondria and plays an important role in promoting cell survival and inhibiting pro-apoptotic proteins.…”

Section: Discussionmentioning

confidence: 99%

<p>Omega-3PUFA Attenuates MNU-Induced Colorectal Cancer in Rats by Blocking PI3K/AKT/Bcl-2 Signaling</p>

Huang

Chun-an

Cai

et al. 2020

OTT

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Background: Omega 3 polyunsaturated fatty acid (Omega-3PUFA) is one of the essential nutrients for human body involved in intracellular metabolic regulation and cell signaling. Previous studies have shown that Omega-3PUFA is involved in the pathogenesis of digestive system tumors, including colorectal cancer (CRC), however, the effects of Omega-3PUFA on CRC has not been fully elucidated. In the current study, we evaluated whether Omega-3PUFA can alleviate N-methyl-N-nitrosourea(MNU) induced CRC in a rat model and illustrated the potential mechanism. Methods: The effects of Omga-3PUFA on MNU-induced colorectal cancer in rats were analyzed by in vivo experiments. The viability, apoptosis, colony formation and invasion of CRC cells treated with Omga-3PUFA were detected by CCK8, flow cytometry, clone formation assay and transwell invasion assay. The expression of apoptosis-related proteins in CRC cells treated with Omga-3PUFA was detected by Western blotting. Finally, after adding PI3K activator, the viability, apoptosis and protein expression of CRC cells treated with Omga-3PUFA were detected by CCK8, flow cytometry and Western blotting. Results: Our results showed that Omega-3PUFA attenuated MNU-induced CRC in rats and inhibited AKT/Bcl-2 signaling in rats. In addition, Omega-3PUFA inhibited CRC cell proliferation and induces CRC cell apoptosis. Moreover, Omega-3PUFA inhibited CRC cell colony formation and invasion, and inhibited PI3K/AKT/Bcl-2 signaling in CRC cells. Furthermore, The effects of Omega-3PUFA on cell proliferation and apoptosis were inhibited by blocking PI3K/AKT signaling. Conclusion: Omega-3PUFA can attenuate MNU-induced colorectal cancer in rats by blocking PI3K/AKT/Bcl-2 signaling, which suggests that Omega-3PUFA may be a potent agent for CRC treatment.

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Effect of cholestasis and NeuroAid treatment on the expression of Bax, Bcl-2, Pgc-1α and Tfam genes involved in apoptosis and mitochondrial biogenesis in the striatum of male rats

Cited by 25 publications

References 87 publications

DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5

DEPDC1B regulates the progression of human chordoma through UBE2T-mediated ubiquitination of BIRC5

Effects of NRF-1 and PGC-1α Cooperation on HIF-1α and Rat Cardiomyocyte Apoptosis Under Hypoxia

<p>Omega-3PUFA Attenuates MNU-Induced Colorectal Cancer in Rats by Blocking PI3K/AKT/Bcl-2 Signaling</p>

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