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CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway

ABSTRACT: the differntial proteins scanning between supernatent of CAFs and NOFs in ovarian cancer.

ORGANISM(S): Homo Sapiens

SUBMITTER: Hua Jiang

PROVIDER: PXD034266 | iProX | Thu Jun 02 00:00:00 BST 2022

REPOSITORIES: iProX

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CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway.

Jin Yunfeng Y Bian Saiyan S Wang Hui H Mo Jiahang J Fei He H Li Li L Chen Tong T Jiang Hua H

Cell death & disease 20220804 8

As the predominant stroma cells of tumor microenvironment (TME), cancer associated fibroblasts (CAFs) are robust tumor player of different malignancies. However, less is known about the regulatory mechanism of CAFs on promoting progression of ovarian cancer (OvCA). In the present study, the conditioned medium of primary CAFs (CAF-CM) from OvCA was used to culture cell lines of epithelial ovarian cancer (EOC), and showed a potent role in promoting proliferation, migration and invasion of cancer c ...[more]

PMID: 35927239

Similar Datasets

CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway.

Project description:As the predominant stroma cells of tumor microenvironment (TME), cancer associated fibroblasts (CAFs) are robust tumor player of different malignancies. However, less is known about the regulatory mechanism of CAFs on promoting progression of ovarian cancer (OvCA). In the present study, the conditioned medium of primary CAFs (CAF-CM) from OvCA was used to culture cell lines of epithelial ovarian cancer (EOC), and showed a potent role in promoting proliferation, migration and invasion of cancer cells. Mass spectrum (MS) analysis identified that Collapsin response mediator protein-2 (CRMP2), a microtubule-associated protein involved in diverse malignancies, derived from CAFs was a key regulator responsible for mediating these cell events of OvCA. In vitro study using recombinant CRMP2 (r-CRMP2) revealed that the protein promoted proliferation, invasion, and migration of OvCA cells through activation of hypoxia-inducible factor (HIF)-1α-glycolysis signaling pathway. The CRMP2 was abundantly expressed in OvCA, with a well correlation with metastasis and poor prognosis, as analyzed from 118 patients' samples. Inhibition of the CRMP2 derived from CAFs by neutralizing antibodies significantly attenuated the tumor size, weights, and metastatic foci numbers of mice in vivo. Our finding has provided a novel therapeutic clue for OvCA based on TME.

| S-EPMC9352901 | biostudies-literature

Cancer-associated fibroblasts-secreted CXCL14-regulated LINC00092 mediates ovarian cancer progression by altering glycolysis

Project description:Epithelial ovarian cancer (EOC) constitutes a major gynecological malignancy, with a reported incidence rate of 3-12/100 000 woman annually. As early symptoms of ovarian cancer are often clinically atypical or absent, the majority of ovarian cancer patients are diagnosed at a late stage, when the five-year survival rate is extremely low. This condition underscores the urgency of early detection of these patients and establishment of new therapeutic targets for successful intervention. Considering that the predominant biological characteristic that differentiates malignant from benign tumors is the ability to metastasize, it is necessary to identify novel metastasis-related molecules for ovarian cancer. In this study, we found that CAFs could significantly increase the metastatic potential of ovarian cancer cells compared with non-cancer associated fibroblasts(NAFs), which is associated with over-expression of CXCL14 in CAFs. We examined the impact of CAF-secreted CXCL14 on the lncRNA expression profiles in ovarian cancer during metastasis. We treated A2780s ovarian cancer cell line with recombinant CXCL14 protein and control respectively and subjected them to Arraystar Human LncRNA microarray v3.0 to profile differential lncRNAs in ovarian cancer upon treatment of CXCL14

2016-06-01 | E-GEOD-82059 | biostudies-arrayexpress

Cancer-associated fibroblasts-secreted CXCL14-regulated LINC00092 mediates ovarian cancer progression by altering glycolysis

2016-06-01 | GSE82059 | GEO

CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway

Project description:To investigate the external CRMP2 function of triggering which signaling pathway in A2780 cells. We treated A2780 cells with human recombinant CRMP2 (r-CRMP2) for RNA-seq to compare deferential genes between two different samples.

2022-08-02 | GSE205385 | GEO

A cancer associated fibroblasts (CAFs) specific gene signature in high grade serous ovarian cancer

Project description:Ovarian cancer is the most lethal malignancy in the United States. In the year 2012, there will be an estimated 22,280 new cases and 15,500 deaths from ovarian cancer in the country (Siegel et al., 2012). While studies on ovarian cancer pathogenesis were mainly focused on the epithelial component of the tumor, understanding in the role of cancer associated fibroblasts (CAFs) in ovarian cancer progression is limited. We hypothesized that comparing the gene expression profiles of different components from laser capture microdissected ovarian tissue will allow us to identify an ovarian CAFs specific gene signature which accounts for the supportive role of CAFs in ovarian cancer progression. In this study, gene expression profiling was completed for 31 cancer stroma samples and 32 samples of epithelial component from high grade serous ovarian cancer patients. 8 microdissected normal ovarian stroma and 6 normal human ovarian surface epithelium (HOSE) samples were also included in the study. By comparing the expression data from cancer stroma against that from normal stroma, cancer cells and HOSE, we identified a set of differential expressed genes in ovarian CAFs which showed correlation with cancer patient survival. Further study on these genes can reveal their roles in ovarian cancer progression and pathogenesis. Ultimately, ovarian CAFs specified genes identified in this study may aid in the classification and enhancement of patient outcome. Transcriptome profiling analyses were performed on 31 laser microdissected cancer associated stroma samples, 32 epithelial tumor samples from high grade serous ovarian cancer patients, 8 microdissected normal ovarian stroma samples and 6 ovarian surface epthelium (HOSE) samples using the Affymetrix human genome U133 Plus 2.0 microarray.

2014-09-11 | E-GEOD-40595 | biostudies-arrayexpress

CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway

Project description:CRMP2 derived from cancer associated fibroblasts facilitates progression of ovarian cancer via HIF-1α-glycolysis signaling pathway

| PRJNA844918 | ENA

A cancer associated fibroblasts (CAFs) specific gene signature in high grade serous ovarian cancer

2014-09-11 | GSE40595 | GEO

Ion Torrent RNA-sequencing of exosomes isolated from ovarian cancer cells, fibroblasts and adipocytes

Project description:We used next-generation sequencing to identify differential microRNA (miRNA) signatures in exosomes isolated from ovarian cancer cells and ovarian cancer-associated fibroblasts (CAFs) and adipocytes (CAAs). We found that a significantly higher levels of miR21 isomiRNAs in exosomes isolated from CAFs and CAAs than in those from ovarian cancer cells.

2016-03-21 | GSE77318 | GEO

Reprogramming of normal fibroblasts into ovarian cancer-associated fibroblasts via non-vesicular paracrine signaling induces an activated fibroblast phenotype

Project description:Cancer-associated fibroblasts (CAFs) are key contributors to ovarian cancer (OC) progression and therapeutic resistance through dysregulation of the extracellular matrix (ECM). CAFs are a heterogenous population derived from different cell types through activation and reprogramming. Current studies rely on uncharacterized heterogenous primary CAFs or normal fibroblasts that fail to recapitulate CAF-like tumor behavior. Here, we present that conditioned media from ovarian cancer lines leads to an increase in the activated state of fibroblasts demonstrated by functional assays and up-regulation of known CAF-related genes and ECM pathways. Phenotypic and functional characterization demonstrated that the conditioned CAFs expressed a CAF-like phenotype, strengthened proliferation, secretory, contractility, and ECM remodeling properties when compared to resting normal fibroblasts, consistent with an activated fibroblast status. Moreover, conditioned CAFs significantly enhanced drug resistance and tumor progression. Critically, the conditioned CAFs resemble a transcriptional signature with involvement of ECM remodeling. The present study provides mechanistic and functional insights about the activation and reprogramming of CAFs in the ovarian tumor microenvironment mediated by nonvesicular paracrine signaling. Moreover, it provides a translational based approach to reprogram normal fibroblasts from both uterine and ovarian origin into CAFs using tumor-derived conditioned media. Using these resources, further development of therapeutics that possess potentiality and specificity towards CAF/ECMmediated chemoresistance in OC are further warranted.

2024-10-30 | GSE280564 | GEO

Carcinoma associated fibroblasts small extracellular vesicles with low miR-7641 promotes breast cancer stemness and glycolysis by HIF-1α.

Project description:Fibroblasts play an important role in cancer development and progression. Small extracellular vesicles (sEVs) are one type of extracellular vesicles, which mediate the interaction between cancer-associated fibroblasts and cancer cells by transferring their contents. However, the roles of sEVs from cancer-associated fibroblasts on breast cancer stem cell properties are largely unraveled. The purpose of this study was to explore the roles of sEVs from cancer-associated fibroblasts on breast cancer progression. The miRNA array data showed a different miRNA profile between CAFs sEVs and normal fibroblasts sEVs. By verification using real-time RT-PCR, the data analysis indicated that miR-7641 levels were lower in sEVs from CAFs compared with NFs. The cellular functions were assayed and the results indicated that CAFs derived sEVs with low miR-7641 levels suppressed breast cancer cell survival, glycolysis, and stem cell properties via the HIF-1α pathway. Collectively, these findings indicated that sEVs from CAFs promoted breast cancer stem cell properties and glycolysis via miR-7641/HIF-1α, which was a possible new way for targeting breast cancer.

| S-EPMC8266840 | biostudies-literature

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