Dataset Information

SUMOylation-Induced Membrane Localization of TRPV1 Suppresses Proliferation and Migration in Gastric Cancer Cells

ABSTRACT: In this work, we elucidate a novel mechanism wherein TRPV1 SUMOylation promotes its membrane expression and activates the TRPV1-Ca2+-AMPK signaling pathway, thereby inhibiting GC cell proliferation and migration. These findings enhance our understanding of the molecular dynamics in gastric cancer and could provide a new theoretical basis for clinical treatment strategies.

ORGANISM(S): Homo Sapiens

SUBMITTER: Yang Yang

PROVIDER: PXD050942 | iProX | Mon Mar 25 00:00:00 GMT 2024

REPOSITORIES: iProX

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SUMOylation-induced membrane localization of TRPV1 suppresses proliferation and migration in gastric cancer cells.

Yang Yang Y Gu Xiaokun X Weng Weiji W Cheng Jinke J Huang Ou O Pan Si-Jian SJ Li Yong Y

Cell communication and signaling : CCS 20240930 1

Gastric cancer (GC) remains a significant health challenge due to its high mortality rate and the limited efficacy of current targeted therapies. A critical barrier in developing more effective treatments is the lack of understanding of specific mechanisms driving GC progression. This study investigates the role of Transient Receptor Potential Vanilloid 1 (TRPV1), a non-selective cation channel known for its high Ca<sup>2+</sup> permeability and tumor-suppressive properties in gastrointestinal c ...[more]

PMID: 39350261

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Project description:Purpose: S100A10 uesed to located in the cell membrane or cytoplasm. However nuclear-located S100A10 was observed in the polyploid tumor giant cells(PGCCs) with daughter cells induced by cobalt chloride(CoCl2). To study the function of nuclear-located S100A10, we performed ChIP-Seq. Methods:LoVo and Hct116 cells were incubated in T25 flasks in RPMI-1640 medium until they reached 80-90% confluence. The cells were treated with 450 μM CoCl2 (Sigma-Aldrich, St. Louis, MO, USA) for 48-72h based on their resistance to hypoxia. After the treatment with CoCl2 was repeated for 3-4 times, there were 20-30% of PGCCs and 70-80% of small-sized daughter cells that originated from PGCCs among the total cells.ChIP assays were performed according to the instructions of the Pierce Magnetic ChIP Kit (Thermo Fisher Scientific, #26157) For data analysis of ChIP DNA, sequencing and library preparation were performed using Novogene Technology Co., Ltd. (Tianjin, China). Raw data (raw reads) of FASTQ format were first processed through in-house PERL scripts, and then reference genome and gene model annotation files were downloaded directly from the genome website. For a specific ChIP-seq binding site, individual reads were mapped to the plus or minus strand and presented significant enrichment. After mapping the reads to the reference genome, the MACS2 version 2.1.0 (model-based analysis of ChIP-seq) peak finding algorithm was used to identify regions of specific IP enrichment over background. A p-value threshold of enrichment of 0.05 was used for all data sets. The interaction between transcription factor or chromatin histone modification and DNA was not random, but they showed some specific sequence preference. MEME 52 and DREME 53 were used to detect the sequence motif, which was used to detect long and short consensus sequences. The position of peak summit around the transcript start sites of genes can predict the interaction sites of proteins and genes. Genes associated with different peaks were identified, and GO and KEGG enrichment analyses were performed. Results:The results showed that 4148 significant ChIP-seq peaked in Hct116-derived PGCCs with daughter cells, and 1380 peaked in LoVo-derived PGCCs with daughter cells. Genes with overlapping peaks were then enriched by Gene Ontology [GO], which revealed that these genes participated in various processes including stimulus, cell migration, and cell motility.Moreover, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed the potential targets involved in metabolic pathways, axon guidance TGF-β signaling pathway, and so on. Conclusions: S100A10 can be modified by SUMOylation in PGCCs and their daughter cells induced by either CoCl2 or chemotherapeutic drugs. SUMO1-modified S100A10 can translocate to the nucleus and regulate the expression of ARHGEF18, PTPRN2, and DEFA3 to promote the proliferation, migration, and invasion of PGCCs and their daughter cells, which may contribute to the poor prognosis in patients with cancer. The discovery of detailed mechanisms of the S100A10 SUMOylation, such as the specific lysine sites involved in SUMOylation and which SUMO E3 ligase regulates the SUMOylation of S100A10 requires further study.

Dataset Information

SUMOylation-Induced Membrane Localization of TRPV1 Suppresses Proliferation and Migration in Gastric Cancer Cells

Publications

SUMOylation-induced membrane localization of TRPV1 suppresses proliferation and migration in gastric cancer cells.

Similar Datasets

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