Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

ABSTRACT: The proteins binding Sema3C and NRP1 in hepatocellular carcinoma cells were analyzed by mass spectrometry

ORGANISM(S): Homo Sapiens

SUBMITTER: Hao Peng

PROVIDER: PXD052807 | iProX | Mon Jun 03 00:00:00 BST 2024

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression.

Peng Hao H Yang Meng M Feng Kun K Lv Qingpeng Q Zhang Yewei Y

Signal transduction and targeted therapy 20240703 1

More than 90% of hepatocellular carcinoma (HCC) cases develop in the presence of fibrosis or cirrhosis, making the tumor microenvironment (TME) of HCC distinctive due to the intricate interplay between cancer-associated fibroblasts (CAFs) and cancer stem cells (CSCs), which collectively regulate HCC progression. However, the mechanisms through which CSCs orchestrate the dynamics of the tumor stroma during HCC development remain elusive. Our study unveils a significant upregulation of Sema3C in f ...[more]

PMID: 38956074

Similar Datasets

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

Project description:Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

| PRJNA1119415 | ENA

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression

Project description:More than 90% of hepatocellular carcinoma (HCC) cases develop in the presence of fibrosis or cirrhosis, making the tumor microenvironment (TME) of HCC distinctive due to the intricate interplay between cancer-associated fibroblasts (CAFs) and cancer stem cells (CSCs), which collectively regulate HCC progression. However, the mechanisms through which CSCs orchestrate the dynamics of the tumor stroma during HCC development remain elusive. Our study unveils a significant upregulation of Sema3C in fibrotic liver, HCC tissues, peripheral blood of HCC patients, as well as sorafenib-resistant tissues and cells, with its overexpression correlating with the acquisition of stemness properties in HCC. We further identify NRP1 and ITGB1 as pivotal functional receptors of Sema3C, activating downstream AKT/Gli1/c-Myc signaling pathways to bolster HCC self-renewal and tumor initiation. Additionally, HCC cells-derived Sema3C facilitated extracellular matrix (ECM) contraction and collagen deposition in vivo, while also promoting the proliferation and activation of hepatic stellate cells (HSCs). Mechanistically, Sema3C interacted with NRP1 and ITGB1 in HSCs, activating downstream NF-kB signaling, thereby stimulating the release of IL-6 and upregulating HMGCR expression, consequently enhancing cholesterol synthesis in HSCs. Furthermore, CAF-secreted TGF-β1 activates AP1 signaling to augment Sema3C expression in HCC cells, establishing a positive feedback loop that accelerates HCC progression. Notably, blockade of Sema3C effectively inhibits tumor growth and sensitizes HCC cells to sorafenib in vivo. In sum, our findings spotlight Sema3C as a novel biomarker facilitating the crosstalk between CSCs and stroma during hepatocarcinogenesis, thereby offering a promising avenue for enhancing treatment efficacy and overcoming drug resistance in HCC.

2024-07-10 | GSE268894 | GEO

Semaphorin 3C (Sema3C) reshapes stromal microenvironment to promote hepatocellular carcinoma progression.

| S-EPMC11220018 | biostudies-literature

Analysis of genes overexpressed in hepatocellular carcinoma

2013-04-27 | GSE46408 | GEO

PHGDH acts as an RNA-binding protein to stabilize PRKCD mRNA and promote hepatocellular carcinoma progression

Project description:PHGDH acts as an RNA-binding protein to stabilize PRKCD mRNA and promote hepatocellular carcinoma progression

2025-05-14 | PXD063943 |

Analysis of genes overexpressed in hepatocellular carcinoma

Project description:Six pairs of hepatocellular carcinoma and their corresponding non-tumrous liver parenchymas were analyzed to identify the genes differentially expressed in hepatocellular carcinoma and nontumorous liver parenchyma. We analyzed mRNA expression pattern of 6 primary hepatocellular carcinomas and their corresponding nontumourous liver parenchyma. The specimens were obtained from a tissue bank in our hospital. All the clinical informations were de-linked from the specimens.

2013-04-27 | E-GEOD-46408 | biostudies-arrayexpress

ALYREF Mediates RNA m5C Modification to Promote Hepatocellular Carcinoma Progression

Project description:ALYREF Mediates RNA m5C Modification to Promote Hepatocellular Carcinoma Progression

| PRJNA916221 | ENA

Determine the role of TXNDC9 in hepatocellular carcinoma progression

Project description:Thioredoxin Domain Containing 9 (TXNDC9) is a member of the thioredoxin family. The exact function of this protein is not known. This experiment is a transcriptiome profiling of TXNDC9 dependent RNA expression in hepatocellular carcinoma cell line HepG2. By compairing the gene expression profile of WT and TXNDC9 knockout, we identified some genes directly or indirectly regulated by TXNDC9 in hepatocellular carcinoma.

2018-12-26 | GSE113400 | GEO

ZMAT2 condensates regulate the alternative splicing of TRIM28 to promote the proliferation of hepatocellular carcinoma cells

Project description:Dysregulation of splicing factor expression plays a crucial role in the progression of hepatocellular carcinoma (HCC). Our research found that the expression level of splicing factor ZMAT2 is increased in HCC, promoting the proliferation of hepatocellular carcinoma cells. RNA-seq data indicated that ZMAT2 regulated exon skipping of mRNA, while RIP-seq data further revealed the binding motifs of ZMAT2. A comprehensive analysis of RNA-seq and RIP-seq data indicateed that ZMAT2 plays a crucial role in the maturation process of TRIM28 mRNA. Deletion of ZMAT2 led to the deletion of 25 bases in exon 11 of TRIM28, ultimately resulting in nonsense-mediated decay (NMD). Previous studies have demonstrated a close association between TRIM28 and the proliferation of hepatocellular carcinoma. Our experiments have revealed that TRIM28 serves as a critical factor for ZMAT2 in facilitating the proliferative process of hepatocellular carcinoma. Studies have demonstrated a close correlation between the mRNA splicing process and the occurrence of phase separation. Our research discovered that ZMAT2 is capable of undergoing phase separation, resulting in the formation of liquid droplet condensates within hepatocellular carcinoma cells. Additionally, it was found that ZMAT2 is able to form protein-nucleic acid condensates with TRIM28 mRNA. In summary, we hypothesize that ZMAT2 and TRIM28 mRNA form protein-nucleic acid condensates, thereby regulating the splicing of TRIM28 mRNA. The augmented expression of ZMAT2 in hepatocellular carcinoma cells results in the upregulation of TRIM28 expression, ultimately driving the proliferation of hepatocellular carcinoma cells.

2024-07-09 | GSE263501 | GEO