The RAS‐PI3K‐AKT‐NF‐κB pathway transcriptionally regulates the expression of BCL2 family and IAP family genes and inhibits apoptosis in fibrous epulis

Jiang, Yangyang; Fang, Bing; Xu, Bo; Chen, Liang

doi:10.1002/jcla.23102

Cited by 19 publications

(19 citation statements)

References 35 publications

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“…The PI3K signalling pathway plays an important role after the overexpression of BCL2. PI3K/AKT/BCL2 is a common apoptotic inhibitory approach in other previous studies 41‐43 . Activated AKT directly promotes the expression of BCL2 to play an anti‐apoptotic role 43 .…”

Section: Discussionmentioning

confidence: 99%

BCL2 enhances survival of porcine pluripotent stem cells through promoting FGFR2

et al. 2020

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Objectives The establishment of porcine pluripotent stem cells (pPSCs) is still a critical topic. However, all pPSCs were failed to contribute to efficient chimeric pig and were extremely sensitive to changes of culture conditions. This study aimed to investigate the role of BCL2 in pPSCs and further explain the mechanism. Materials and Methods Porcine BCL2 gene was cloned and overexpressed in porcine induce pluripotent stem cells (piPSCs). Digital RNA‐seq was performed to explain the mechanism of anti‐apoptosis. Finally, the cells carrying BCL2 were injected into mouse early embryo to evaluate its chimeric ability. Results Here, we found that overexpression of porcine BCL2 gene significantly improved the survivability of piPSCs and the efficiency of embryonic chimerism, and did not wreck the pluripotency of piPSCs. Furthermore, the Digital RNA‐seq analysis revealed that BCL2, as a downstream gene of the PI3K signal pathway, enhanced the expression of PI3K signal pathway receptors, such as FGFR2, and further promoted oxidoreductases activity and lipid metabolism, thus maintaining the survival and pluripotency of piPSCs. Conclusion Our data not only suggested that porcine BCL2 gene could enhance the survivability and chimeric ability of pPSCs, but also explained the positive feedback mechanism in this process, providing strong support for the chimeric experiment of pPSCs.

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Section: Discussionmentioning

confidence: 99%

BCL2 enhances survival of porcine pluripotent stem cells through promoting FGFR2

et al. 2020

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“…Next, increasing resistance to tumor cell death by immune cells also could induce immune evasion including increased expression of cellular FLICE-like inhibitory protein (cFLIP) or inhibitor of apoptosis proteins (IAPs). NF-κB pathway could positively regulate expression of IAP family, leading to the proliferation and apoptosis inhibition 50 , while up-regulation of RNA demethylase ALKBH5 could improve the activation of the NF-κB pathway in carcinogesis 51 . The RNA demethylase ALKBH5 could increase the IAPs expression by activating the NF-κB signals in tumor cells to resist the immune cells.…”

Section: Introductionmentioning

confidence: 99%

Emerging role of RNA modification N6-methyladenosine in immune evasion

et al. 2021

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The innate and adaptive immune cells have complex signaling pathways for sensing and initiating immune responses against disease. These pathways are interrupted at different levels to occur immune evasion, including by N6-methyladenosine (m6A) modification. In this review, we discuss studies revealing the immune evasion mechanism by m6A modification, which underlies the retouching of these signaling networks and the rapid tolerance of innate and adaptive immune molecules during disease. We also focus on the functions of m6A in main chemokines regulation, and their roles in promotive and suppressive immune cell recruitment. We then discuss some of the current challenges in the field and describe future directions for the immunological mechanisms of m6A modification.

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“…COL6A6 has been reported to be down-regulated in breast cancer [27][28][29] . Significant down-regulation of COL6A5 has been proved in esophageal squamous cell carcinoma 30 and fibrous epulis 31 . Wang and the colleagues has found that collagen type VI may interacts with ROBO2 in esophageal squamous cell carcinoma development, and ROBO2 serves as a tumor suppressor during malignant process 32 .…”

Section: Discussionmentioning

confidence: 99%

Collagen type VI α5 gene variations may predict the risk of lung cancer development in Chinese Han population

Duan

Liu

Sun

et al. 2020

Sci Rep

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the abundant expression of collagen type VI α5 (COL6A5) exists in lung tissue, and its role in lung cancer is still unknown. We performed a genetic association study with an attempt to detect the relationships between single nucleotide polymorphisms (Snps) in COL6A5 and lung cancer predisposition in chinese Han population. We finally selected six tag-SNPs to determine their genotypes among 510 lung cancer patients and 495 healthy controls with the MassARRAY platform. The associations of SNPs and lung cancer risk were estimated by logistic regression method with adjustment for confounding factors. two available databases were used for gene expression and prognosis analysis. COL6A5 rs13062453, rs1497305, and rs77123808 were significantly associated with the risk of lung cancer in the whole population or stratified subgroups (p < 0.05). Among them, COL6A5 rs13062453 and rs1497305 were also linked to the susceptibility of lung adenocarcinoma. Additionally, rs1497305 was found to be strongly related to the TNM staging under five genetic models (p < 0.05). Results from databases suggested the important role of COL6A5 in lung cancer development. COL6A5 polymorphisms rs13062453, rs1497305 and rs77123808 were associated with lung cancer risk in Chinese Han population. These findings first yield new insight of COL6A5 in lung cancer.The incidence and mortality rates of lung cancer rank first worldwide, with 2,093,876 (11.6% of total cancer patients) new cases and 1,761,007 (18.4% of total cancer deaths) deaths occurred globally in 2018 1 . Considering the sex-distribution difference, lung cancer is the leading cause of cancer incidence (1,368,524 new cases) and death (1,184,947 deaths) among males, accounting for approximately 14.4% new cases and 22.0% deaths respectively, and the third prevalent cancer (725,352 new cases, 8.4%) with second fatality rate (576,060 deaths, 13.8%) among females 1 . The morbidity and mortality of lung cancer is very high in China, even worse, continue rising in recent years 2 . Previous epidemiological studies have reported a dramatical increase of crude incidence of lung cancer among Chinese from 2000 to 2014, which reached 57.13 per 100,000 in 2014 (74.31 per 100,000 in males and 39.08 per 100,000 in females) 2,3 . In the same year, the estimated mortality rate of lung cancer deaths is 45.80 per 100,000 (61.10 per 100,000 in males and 29.71 per 100,000 in females) 3 . Multiple etiological analyses have found that external risk factors such as smoking, air pollution and occupational exposure contribute to the lung tumorigenesis 4-6 . Moreover, researchers have emphasized that genetic factors play critical roles in the development of lung cancer as well. Nowadays, accumulating evidence has elucidated that genetic polymorphisms are risk markers that can mediate individual susceptibility to lung cancer 7-11 . These findings also provide multiple promising indicators that pave the road for individual cancer risk assessment. Therefore, exploring these novel factors is a vital step which not only re...

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The RAS‐PI3K‐AKT‐NF‐κB pathway transcriptionally regulates the expression of BCL2 family and IAP family genes and inhibits apoptosis in fibrous epulis

Cited by 19 publications

References 35 publications

BCL2 enhances survival of porcine pluripotent stem cells through promoting FGFR2

BCL2 enhances survival of porcine pluripotent stem cells through promoting FGFR2

Emerging role of RNA modification N6-methyladenosine in immune evasion

Collagen type VI α5 gene variations may predict the risk of lung cancer development in Chinese Han population

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