Knocking down GALNT6 promotes pyroptosis of pancreatic ductal adenocarcinoma cells through NF-κB/NLRP3/GSDMD and GSDME signaling pathway

Ding, Mengyang; Liu, Jingyu; Lv, Honghui; Zhu, Yanlin; Chen, Yumiao; Hui, Pei; Fan, Sairong; Chen, Xiaoming

doi:10.3389/fonc.2023.1097772

Cited by 11 publications

(7 citation statements)

References 46 publications

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“…37 For example, GALNT6 serves as a carcinogenic role in pancreatic ductal adenocarcinoma cells through regulation pyroptosis, which is mediated via NF-κB/NLRP3/GSDMD and GSDME signaling. 38 FABP4 is involved in inducing macrophage pyroptosis via NLRP3/IL-1β axis, thereby promoting the migration, invasion, and metastasis in pancreatic cancer cells. 39 Hydrogen inhibits endometrial cancer progression, which is linked to pyroptotic pathway via ROS/ NLRP3/caspase-1/GSDMD.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence has demonstrated that pyroptosis contributes to the onset and progression of cancers, in which the NLRP3 inflammasome‐mediated pathway is particularly highlighted 37 . For example, GALNT6 serves as a carcinogenic role in pancreatic ductal adenocarcinoma cells through regulation pyroptosis, which is mediated via NF‐κB/NLRP3/GSDMD and GSDME signaling 38 . FABP4 is involved in inducing macrophage pyroptosis via NLRP3/IL‐1β axis, thereby promoting the migration, invasion, and metastasis in pancreatic cancer cells 39 .…”

Section: Discussionmentioning

confidence: 99%

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KIF23 promotes cervical cancer progression via inhibiting NLRP3‐mediated pyroptosis

Liu,

Xie,

et al. 2024

The FASEB Journal

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BackgroundCervical cancer (CC), closely linked to persistent human papillomavirus infection, represents a major health problem for women worldwide. The objective of this study is to elucidate KIF23's role in the development of CC and its regulatory mechanism.MethodsThe bioinformatics methods were utilized to extract pyroptosis‐associated differentially expressed genes (DEGs) and pivot genes from the GSE9750 and GSE63678 datasets, followed by immune infiltration analysis and quantification of these genes' expression. The effects of kinesin family member 23 (KIF23) were verified through functional experiments in vitro and a mouse xenograft model. The NLPR3 activator, nigericin, was applied for further analyzing the potential regulatory mechanism of KIF23 in CC.ResultsA total of 8 pyroptosis‐related DEGs were screened out, among which 4 candidate core genes were identified as candidate hub genes and confirmed upregulation in CC tissues and cells. These genes respectively showed a positive correlation with the infiltration of distinct immune cells or tumor purity. Downregulation of KIF23 could suppress the proliferation, migration, and invasion abilities in CC cells and tumorigenesis through enhancing pyroptosis. Conversely, KIF23 overexpression accelerated the malignant phenotypes of CC cells and inhibited pyroptosis activation, which was blocked by nigericin treatment.ConclusionsKIF23 may play an oncogenic role in CC progression via inhibition of the NLRP3‐mediated pyroptosis pathway.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

KIF23 promotes cervical cancer progression via inhibiting NLRP3‐mediated pyroptosis

Liu,

Xie,

et al. 2024

The FASEB Journal

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“…The peptide N-acetylgalactosaminyltransferase-6 (GALNT6) is highly expressed in pancreatic ductal adenocarcinomas, and it has been noted that knockdown of GALNT6 leads to increased activation of the NF-κB signaling pathway in pancreatic ductal adenocarcinoma cells as evidenced by an increase in NF-κB phosphorylation. A decrease in glycosylation was also observed, and the above changes combined to achieve the effect of inhibiting tumor cell proliferation [54] . In addition, steroidal saponins are a class of natural compounds, and many of them have potential bioactivities and pharmacological effects.…”

Section: Pancreatic Cancermentioning

confidence: 97%

Progress and perspectives of cellular pyroptosis in digestive tract tumors

2023

FMSR

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Cellular pyroptosis, a novel mode of cell death in recent years, is triggered by cysteine asparaginase. Distinguished from traditional apoptosis and necrosis, this mode of cell death is characterized by the activation of inflammatory vesicles and the release of inflammatory factors. Its unique mechanism and morphological changes have attracted increasing attention regarding their role in the development and progression of gastrointestinal (GI) tumors. This has provided new insights and potential strategies for tumor prevention and treatment. Among these strategies, intervening in the process of cellular pyroptosis has been considered a promising approach to inhibit tumor growth. This review aims to explore the mechanism of cellular pyroptosis, its role in GI tumors, and its potential applications in therapy.

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“…Western blotting was performed as previously described [50]. The primary antibodies were used in Tab.S3.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…Quantitative real-time PCR was performed as previously described [50]. The primer sequences were used in Tab.S2.…”

Section: Quantitative Real-time Pcrmentioning

confidence: 99%

FUT2 promotes colorectal cancer metastasis by reprogramming fatty acid metabolism via YAP/TAZ signaling and SREBP-1

Chen,

Dong,

Zhang

et al. 2024

Preprint

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Colorectal cancer (CRC) ranks as the second most lethal cancer worldwide because of high rate of metastasis, approximately 20% of CRC patients have metastases at initial diagnosis. Metabolism reprogramming, as a universal feature for cancer cells, is considered to be associated with metastasis. We have previously demonstrated that fucosyltransferase 2 (FUT2) functions as a potent oncogene in CRC, and promotes the development and malignancy of CRC cells, however, the underlying mechanism remains unclear. Here, bioinformatic analysis indicated that FUT2 was related to malignant phenotype and fatty acid metabolism in CRC. FUT2 knockdown decreased glucose uptake and de novo fatty acid synthesis, which in turn inhibited the proliferation and metastasis of CRC cells. Mechanistically, FUT2 promotes YAP1 nuclear translocation and concurrently stabilizing mSREBP-1 by fucosylation, thus promoting de novo fatty acid synthesis in CRC cells. Furthermore, a prognostic model, constructed based on YAP1, SREBP-1, FUT2, and FASN, has high accuracy in the OS of CRC patients. In summary, this study demonstrates that FUT2 reprograms fatty acid metabolism of CRC cells via Hippo signaling pathway and SREBP-1. The findings imply that FUT2 might be a potential target for the development of therapeutic strategies against CRC.

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Knocking down GALNT6 promotes pyroptosis of pancreatic ductal adenocarcinoma cells through NF-κB/NLRP3/GSDMD and GSDME signaling pathway

Cited by 11 publications

References 46 publications

KIF23 promotes cervical cancer progression via inhibiting NLRP3‐mediated pyroptosis

KIF23 promotes cervical cancer progression via inhibiting NLRP3‐mediated pyroptosis

Progress and perspectives of cellular pyroptosis in digestive tract tumors

FUT2 promotes colorectal cancer metastasis by reprogramming fatty acid metabolism via YAP/TAZ signaling and SREBP-1

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