Acid/bile exposure triggers TRAIL-mediated apoptosis in esophageal cancer cells by suppressing the decoy receptors and c-FLIPR

Meng, Xiemei; Chang, Zhiheng; Che, Na; Wu, Jinbao; Dang, Tong; Chai, Jianyuan

doi:10.1016/j.biocel.2020.105736

Cited by 7 publications

(9 citation statements)

References 23 publications

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“…were increased in periodontitis patients. A cohort study found that advanced periodontitis was associated with elevated risks of EC [ 65 ], and many kinds of research [ 66 , 67 ] proved that a high level of oral IL-17 promoted the development of periodontitis via its pro-inflammatory and osteoclastogenic properties [ 68 ]. These results could assume that W-thick and Y-thin coatings may represent the oral pathogenic trait and inflammation, and simultaneously reflect the progress of upper digestive tract cancer.…”

Section: Discussionmentioning

confidence: 99%

Microbial Characteristics of Common Tongue Coatings in Patients with Precancerous Lesions of the Upper Gastrointestinal Tract

Kang

Lü

Xiao

et al. 2022

Journal of Healthcare Engineering

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The tongue coating (TC) microbiota, a crucial component of the tongue coating, illustrates a huge microbial percentage of the body that mostly includes actinobacteria, bacteroides, firmicutes, and fusobacteria. The TC microbiota is closely related to the development of upper gastrointestinal malignancies, such as oral, gastric, and esophageal cancer. Nonetheless, the microbiological characteristics of common TCs in individuals with precancerous lesions of the upper gastrointestinal tract are still unclear. Herein, we designed a case-control study, recruiting 153 PLUGT patients with four different types of TCs, including 47 white-thin, 19 white-thick, 47 yellow-thin, and 40 yellow-thick, as well as 47 volunteers as controls. To analyze microbial characteristics, 16S rRNA microbiome approaches were used. An enzyme-linked immunosorbent assay (ELISA) was employed to assess serum IL-17A and total bile acid (TBA). According to the obtained results, Leptotrichia was found to be a promising biomarker for thin as well as thick yellow coatings. In comparison to the control TC microbiota, 39 different genera developed commensal networks in common TCs. Lachnoanaerobaculum and pseudonocardia were the most striking core bacteria. Lachnoanaerobaculum positively correlated with Leptotrichia in W-thin and Y-thick coatings, with actinomyces and methylobacterium in Y-thin coatings, with Campylobacter in Y-thick coatings, and with Bradyrhizobium in W-thick and Y-thick coatings. Serum IL-17A levels were greater in cases with W-thin coating than in controls, and serum IL-17A was positively linked with Parvimonas in patients with W-thick or Y-thin coating. In Y-thin coating, the oral dominating bacteria Streptococcus was negatively linked with serum TBA. Taken together, the promoted bacteria were found to be synergistically proliferative in the TCs of PLUGT patients. The diverse TCs had distinct bacterial commensal networks, whereas the common TCs were linked by specific bacteria to serum IL-17A and TBA.

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Section: Discussionmentioning

confidence: 99%

Microbial Characteristics of Common Tongue Coatings in Patients with Precancerous Lesions of the Upper Gastrointestinal Tract

Kang

Lü

Xiao

et al. 2022

Journal of Healthcare Engineering

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“…The c-FLIP proteins regulate the activation of procaspase-8a/b. 118 This regulation is located on the DED filaments. There are 3 c-FLIP isoforms: c-FLIP L (Long), c-FLIP S (Short), and c-FLIP R (Raji).…”

Section: 26mentioning

confidence: 99%

“…Another major regulator of caspase activation is c‐FLIP. The c‐FLIP proteins regulate the activation of procaspase‐8a/b 118 . This regulation is located on the DED filaments.…”

Section: Mechanisms Of Regulation Of Apoptosismentioning

confidence: 99%

“…This regulation is located on the DED filaments. There are 3 c‐FLIP isoforms: c‐FLIP L (Long), c‐FLIP S (Short), and c‐FLIP R (Raji) 118 . c‐FLIP L has a proapoptotic function at an intermediate concentration by forming catalytically active procaspase‐8/c‐FLIP L heterodimers and stabilizing the active center of procaspase‐8 119 .…”

Section: Mechanisms Of Regulation Of Apoptosismentioning

confidence: 99%

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Review of cancer cell resistance mechanisms to apoptosis and actual targeted therapies

Kulbay

Paimboeuf

Ozdemir

et al. 2021

J of Cellular Biochemistry

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The apoptosis pathway is a programmed cell death mechanism that is crucial for cellular and tissue homeostasis and organ development. There are three major caspase‐dependent pathways of apoptosis that ultimately lead to DNA fragmentation. Cancerous cells are known to highly regulate the apoptotic pathway and its role in cancer hallmark acquisition has been discussed over the past decades. Numerous mutations in cancer cell types have been reported to be implicated in chemoresistance and treatment outcome. In this review, we summarize the mutations of the caspase‐dependant apoptotic pathways that are the source of cancer development and the targeted therapies currently available or in trial.

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“…Some EAC cells (e.g., OE19 and FLO-1) can live through chronic acid attacks (pH 4.5) but die of TRAIL-mediated apoptosis when bile is present. 49 Under acidic conditions, these cells overexpress the decoy receptors to interfere with TRAIL signaling. In addition, c-FLIP R is upregulated to block CASP8 activation.…”

Section: Acid/bile Exposure Triggers Trail-mediated Apoptosis In Some...mentioning

confidence: 99%

The Role of CCN1 in Esophageal Adenocarcinoma: What We Have Learned From the Lab

et al. 2022

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Background: Esophageal cancer is one of the most common and deadliest cancers in the world, particularly esophageal adenocarcinoma. There has never been a special drug to treat it. Purpose: This article summarizes the work that we have done in our laboratory about the role of CCN1 in esophageal cancer and gives a new perspective of CCN1 biology. Research Design: This is a review article. Study Sample: The work was done using validated cell lines and fixed human tissue slides. Data Collection and Analysis: This is a review article, therefore, no data collection or analysis was involved. Results: CCN1 is a matricellular protein supporting adhesion, migration, and survival in normal cells, but in the esophageal cancer cells, it induces TRAIL-mediated apoptosis. CCN1 promotes TRAIL and its death receptor expression but downregulates the decoy receptors and survivin in a p53-dependant manner. It was thought that CCN1 relies on TNF to induce apoptosis, but our study found that these two molecules antagonize each other. CCN1 promotes TNFR1 cleavage and uses the soluble product to block TNF signaling, while TNF upregulates PGLYRP1 to overcome this obstacle because PGLYRP1 is a secreted protein that competes with TNF for TNFR1 binding. As a result, when CCN1 and TNF are present together in the vicinity of esophageal tumors, they cancel each other out. Conclusions: Based on our laboratory study, CCN1 has much potential to be a candidate for the treatment of esophageal cancer.

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Acid/bile exposure triggers TRAIL-mediated apoptosis in esophageal cancer cells by suppressing the decoy receptors and c-FLIPR

Cited by 7 publications

References 23 publications

Microbial Characteristics of Common Tongue Coatings in Patients with Precancerous Lesions of the Upper Gastrointestinal Tract

Microbial Characteristics of Common Tongue Coatings in Patients with Precancerous Lesions of the Upper Gastrointestinal Tract

Review of cancer cell resistance mechanisms to apoptosis and actual targeted therapies

The Role of CCN1 in Esophageal Adenocarcinoma: What We Have Learned From the Lab

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