&lt;p&gt;Autophagy-Related Beclin 1 and Head and Neck Cancers&lt;/p&gt;

Hu, Yang-Jie; Zhong, Jiang-Tao; Gong, Liang; Sicong, Zhang; Zhou, Shui‐Hong

doi:10.2147/ott.s256072

Cited by 23 publications

(22 citation statements)

References 129 publications

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“…15,16 As reported, the expression of autophagy-related gene Beclin-l in burn wounds was significantly increased, and increased autophagy was found to be helpful for wound healing. 17 However, excessive autophagy induced apoptosis and led to delayed wound healing. 18 Our experimental results also support this view.…”

Section: Discussionmentioning

confidence: 99%

Advanced oxidation protein products mediate human keratinocytes apoptosis by inducing cell autophagy through the mTOR–Beclin‐1 pathway

Ding

Liu

Tan

et al. 2022

Cell Biochemistry & Function

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Excessive keratinocyte apoptosis leads to impaired wound healing. Recently, advanced oxidation protein products (AOPP) have been recognized as a marker of oxidative stress and a potent inducer of apoptosis. Previously, we have demonstrated that extracellular AOPP accumulation induced keratinocyte apoptosis, and we discovered that autophagy was involved. To further elucidate the role and mechanism of autophagy in AOPP‐induced‐apoptosis of keratinocytes, we treated HaCaT cells with increasing concentrations of AOPP‐human serum albumin or with AOPP‐human serum albumin for increasing durations. Cyto‐ID solution staining was used to assess cell autophagy using confocal laser scanning microscopy. Autophagy‐related protein interactions were investigated using western blot analysis. Exposure of HaCaT cells to AOPP decreased the expression of mammalian target of rapamycin (mTOR) and increased the expression of autophagy‐related proteins Beclin‐l and LC3, and eventually led to autophagy. Furthermore, an autophagy agonist significantly decreased the expression of apoptosis‐related proteins. Taken together, we showed that accumulation of extracellular AOPP induced autophagy in HaCaT cells via a reactive oxygen species‐dependent, mTOR–Beclin‐1‐mediated pathway, and that excessive autophagy‐mediated apoptosis, which resulted in delayed wound healing.

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Section: Discussionmentioning

confidence: 99%

Advanced oxidation protein products mediate human keratinocytes apoptosis by inducing cell autophagy through the mTOR–Beclin‐1 pathway

Ding

Liu

Tan

et al. 2022

Cell Biochemistry & Function

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“…The need for more sensitive molecular predictors of survival in HCC cases had been challenged in many studies with unsatisfactory impacts. The autophagy gene, Beclin-1, had been studied in stomach, ovaries, esophagus, and colon cancers (Hu et al, 2020). Over-expression of Beclin-1 had been demonstrated in pancreatic and nasopharyngeal cancer (Hu et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Altered Protein and Gene Expression of Beclin-1 Correlates with Poor Prognosis of Hcv-Associated Hepatocellular Carcinoma in Egyptian Patients

Ehsan

Mosbeh

Elkhadry

et al. 2021

Asian Pac J Cancer Prev

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“…In our study, ATG4, ATG5, and ATG8 gene levels were upregulated in each iAs 3+ dose group. Moreover, Beclin-1 is a key regulator of autophagy; it promotes the transformation of LC3-I to LC3-II, thereby re ecting autophagy activation 39 . Previous evidence has suggested mTOR is a regulatory autophagy inhibitor, promotes Beclin-1 release, and is an important regulator in anabolism and catabolism, cell growth, and proliferation 9 .…”

Section: The Effects Of Naaso 2 On Autophagy Levels Lx-2 Cellsmentioning

confidence: 99%

The Effects of Inorganic Arsenic On Apoptosis and Autophagy in Human Hepatic Sellate Cells

Huang

et al. 2022

Preprint

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Endemic arsenism is a major disease concern in China, with arsenic poisoning and induced potential lesions key issues on a global level. The liver is the main target organ where arsenic is metabolized; chronic exposure to arsenic-induced liver fibrosis is also closely related to autophagy, however, the exact mechanisms are remain unclear. In this study, we explored the effects of NaAsO2 on apoptosis and autophagy in human hepatic stellate cells(HSC). We established a fibrosis model in the HSC line, LX-2 which was exposed to NaAsO2 for 24h, 48h, and 72h. Cells were then transfected using an autophagy double-labeled RFP-GFP-LC3 adenoviral plasmid. Laser confocal microscopy indicated significant infection efficiencies and autophagy in LX-2. Flow cytometry was also used to investigate the effects of different NaAsO2 doses on apoptosis. NaAsO2 treatment upregulated the expression of autophagic markers, including microtubule-associated protein light chain A/B(LC3), ubiquitin binding protein(SQSTM-1/P62), autophagy related genes(ATGs), recombinant human autophagy effector protein (Beclin-1), and B cell lymphoma-2(BCL-2), but downregulated mammalian target of rapamycin(mTOR). Also, α-smooth muscle actin(α-SMA) expression was significantly upregulated in all NaAsO2 groups. Furthermore, mTOR silencing via 3-methyladenine(3-MA) altered NaAsO2 induced autophagy, LC3, Beclin-1, and SQSTM-1/P62 expression were all upregulated in both NaAsO2 and 3-MA-iAs groups. Altogether, NaAsO2 induced HSC autophagy via apoptotic pathways. 3-MA inhibited LX-2 activity and reduced NaAsO2-induced autophagy which may inhibit fibrosis progression caused by this toxin.

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<p>Autophagy-Related Beclin 1 and Head and Neck Cancers</p>

Cited by 23 publications

References 129 publications

Advanced oxidation protein products mediate human keratinocytes apoptosis by inducing cell autophagy through the mTOR–Beclin‐1 pathway

Advanced oxidation protein products mediate human keratinocytes apoptosis by inducing cell autophagy through the mTOR–Beclin‐1 pathway

Altered Protein and Gene Expression of Beclin-1 Correlates with Poor Prognosis of Hcv-Associated Hepatocellular Carcinoma in Egyptian Patients

The Effects of Inorganic Arsenic On Apoptosis and Autophagy in Human Hepatic Sellate Cells

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