Bcl-2/Caspase 3 mucosal imbalance favors T cell resistance to apoptosis in dogs with inflammatory bowel disease

Ae, Jergens; Young, Jik; Moore, David; Wang, Chong; Hostetter, Jesse M.; Augustine, Laura A.; Allenspach, Karin; Schmitz, Silke Salavati; Mosher, Curtis

doi:10.1016/j.vetimm.2014.01.004

Cited by 14 publications

(9 citation statements)

References 34 publications

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“…This finding agrees with two studies that evaluated apoptosis in canine IBD, where the expression of Bcl-2 was greater in the duodenum and colon of healthy control dogs versus dogs with IBD and greater numbers of Bcl-2 cells were found in the colon of healthy control dogs compared to dogs with IBD. It is therefore possible that this could be the reason for the miR-16 increase in the colonic mucosa that was detected in our study [39,40]. In mice, miR-21 could be involved in the pathogenesis of IBD through at least 3 different mechanisms targeting epithelial barrier function, apoptosis and fibrosis [41].…”

Section: Discussionmentioning

confidence: 74%

Colonic mucosal and serum expression of microRNAs in canine large intestinal inflammatory bowel disease

et al. 2020

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Background: Canine inflammatory bowel disease (IBD) is a group of chronic gastrointestinal (GI) disorders of still largely unknown etiology. Canine IBD diagnosis is time-consuming and costly as other diseases with similar signs should be initially excluded. In human IBD microRNA (miR) expression changes have been reported in GI mucosa and blood. Thus, there is a possibility that miRs may provide insight into disease pathogenesis, diagnosis and even treatment of canine IBD. The aim of this study was to determine the colonic mucosal and serum relative expression of a miRs panel in dogs with large intestinal IBD and healthy control dogs. Results: Compared to healthy control dogs, dogs with large intestinal IBD showed significantly increased relative expression of miR-16, miR-21, miR-122 and miR-147 in the colonic mucosa and serum, while the relative expression of miR-185, miR-192 and miR-223 was significantly decreased. Relative expression of miR-146a was significantly increased only in the serum of dogs with large intestinal IBD. Furthermore, serum miR-192 and miR-223 relative expression correlated to disease activity and endoscopic score, respectively. Conclusion: Our data suggest the existence of dysregulated miRs expression patterns in canine IBD and support the potential future use of serum miRs as useful noninvasive biomarkers.

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Section: Discussionmentioning

confidence: 74%

Colonic mucosal and serum expression of microRNAs in canine large intestinal inflammatory bowel disease

et al. 2020

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“…Additionally, the miR-340 overexpression was shown to affect the levels of 4 apoptotic factors – pro-CASP3, cleaved CASP3, BCL2, and BAX – which possess the corresponding changes of promoted cell apoptosis. The 4 factors are widely used as indicators for cell apoptosis in numerous studies; BCL2 is an anti-apoptosis factor, and CASP3 and BAX are pro-apoptosis factors [30,31]. The up-regulated pro-CASP3, cleaved-CASP3, and BAX, as well as the down-regulation of BCL2 by miR-340 further confirmed the induced apoptosis in miR-340-transfected SGC-7901 cells.…”

Section: Discussionmentioning

confidence: 82%

miR-340 Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cell Line SGC-7901, Possibly via the AKT Pathway

Yu¹,

Wang

Chen³

et al. 2017

Med Sci Monit

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BackgroundGastric cancer is among the most common types of cancer, with high morbidity and mortality. MicroRNAs (miRNAs) play vital roles in the tumorigenesis and biology of gastric cancer. This study aimed to reveal the role of miR-340 in gastric cancer cell proliferation and apoptosis and to elucidate the potential mechanisms.Material/MethodsHuman gastric cancer cells SGC-7901 were used in this study for cell transfection with miR-340 mimic or inhibitor. After transfection, cell viability, proliferation, and apoptosis were examined by MTT, BrdU, and flow cytometry assays, respectively. The protein level changes of p27, p21, Caspase 3 (CASP3), B cell lymphoma 2 (BCL2), BCL2-associated X protein (BAX), and v-AKT murine thymoma viral oncogene (AKT) were detected by Western blot.ResultsOverexpression of miR-340 significantly reduced cell viability and proliferation (P<0.01), and induced cell apoptosis (P<0.01) of SGC-7901. miR-340 elevated the protein level of cell cycle inhibitor p27, but did not affect the level of p21. Apoptosis-related factors pro-CASP3, cleaved-CASP3, and BAX were promoted, and BCL2 was inhibited by miR-340. miR-340 also suppressed the phosphorylation of AKT. Opposite effects were detected when SGC-7901 cells were transfected with miR-340 inhibitor.ConclusionsThese results indicate that miR-340 can inhibit proliferation and induce apoptosis of SGC-7901 cells, suggesting its roles in protecting against gastric cancer. The roles of miR-340 in gastric cancer cells may be associated with its regulation of the AKT pathway. Thus, miR-340 may be a potential therapeutic strategy for gastric cancer treatment.

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“…Extensive studies (10,18,20,21,24) have demonstrated that agents that prevent tumorigenesis do so by disorganizing tumor initiation, proliferation, migration and invasion via cell death pathways, including apoptosis and autophagy. As important regulatory factors in the process of cell apoptosis, Bcl-2 family members are divided into two groups: Anti-apoptotic proteins (Bcl-2) and pro-apoptotic proteins (Bax) (26,27). Caspase-3 is downstream of the activator caspases.…”

Section: Discussionmentioning

confidence: 99%

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

Zhang

Wang

Sun³

et al. 2018

Mol Med Report

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Isoliquiritigenin (ISL) is a ﬂavonoid extracted from licorice root, which is known to serve important antitumor roles in numerous types of cancers; however, its effect on gastric cancer remains to be elucidated. The present study aimed to explore the roles and underlying mechanisms of ISL in MKN28 gastric cancer cells. MKN28 cell proliferation was measured using the Cell Counting Kit‑8 (CCK8) assay. A Transwell assay was used to determine the effects of ISL on the migration and invasion of MKN28 cells. Apoptosis was assessed by flow cytometry, and the expression levels of apoptosis‑, autophagy‑ and signaling pathway‑related proteins were detected by western blot analysis. The results of the CCK8 assay demonstrated that ISL significantly inhibited the proliferation of MKN28 cells (P<0.05). Transwell assays demonstrated that the migration and invasion of MKN28 cells were significantly inhibited following treatment with ISL (P<0.05). Flow cytometric analysis indicated that ISL induced apoptosis of MKN28 cells. In addition, western blot analysis revealed that the ratio of microtubule‑associated proteins 1A/1B light chain 3B (LC3)II/LC3I was upregulated, as was Beclin 1 expression; however, p62 was downregulated following ISL pretreatment, thus suggesting that ISL triggered autophagy in MKN28 cells. In addition, the phosphorylation levels of protein kinase B (AKT) and mammalian target of rapamycin (mTOR) were significantly reduced following ISL treatment. These results indicated that ISL may influence apoptosis and autophagy in MKN28 cells by suppressing the phosphoinositide 3‑kinase/AKT/mTOR signaling pathway. In conclusion, the findings of the present study suggested that ISL may inhibit MKN28 cell proliferation, migration and invasion by inducing apoptosis and autophagy, implying potential as a therapeutic agent for gastric cancer.

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Bcl-2/Caspase 3 mucosal imbalance favors T cell resistance to apoptosis in dogs with inflammatory bowel disease

Cited by 14 publications

References 34 publications

Colonic mucosal and serum expression of microRNAs in canine large intestinal inflammatory bowel disease

Colonic mucosal and serum expression of microRNAs in canine large intestinal inflammatory bowel disease

miR-340 Inhibits Proliferation and Induces Apoptosis in Gastric Cancer Cell Line SGC-7901, Possibly via the AKT Pathway

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

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