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Expression data from FSTL1 antibody treatment for 6 hours in CL1-0 lung cancer cell line.

ABSTRACT: We demonstrate that FSTL1 down-regulation shRNAs significantly increased cell migration and invasion in lung cancer cell lines in vitro, as well as in lung metastases in vivo We used microarrays to analyze the FSTL1 regulated gene expression underlying invasion-metastasis cascade.

ORGANISM(S): Homo sapiens

PROVIDER: GSE79682 | GEO | 2021/03/31

REPOSITORIES: GEO

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Expression data from ALDOA overexpression in CL1-0 lung cancer cell line and ALDOA knockdown in CL1-5 lung cancer cell line.

Project description:We demonstrate that ALDOA down-regulation shRNAs significantly reduced cell migration and invasion in highly invasive lung cancer cell lines in vitro, as well as in lung metastases in vivo We used microarrays to analyze the ALDOA regulated gene expression underlying invasion-metastasis cascade.

2019-12-31 | GSE68716 | GEO

Expression data from AK4 overexpression in CL1-0 lung cancer cell line and AK4 knockdown in CL1-5 lung cancer cell line

2012-12-03 | GSE37903 | GEO

Expression data from PSAT1 overexpression in CL1-0 lung cancer cell line and PSAT1 knockdown in CL1-5 lung cancer cell line.

Project description:We demonstrate that PSAT1 down-regulation shRNAs significantly reduced cell migration and invasion in highly invasive lung cancer cell lines in vitro, as well as in lung metastases in vivo We used microarrays to analyze the PSAT1 regulated gene expression underlying invasion-metastasis cascade.

2020-12-29 | GSE75961 | GEO

Expression data from AK4 overexpression in CL1-0 lung cancer cell line and AK4 knockdown in CL1-5 lung cancer cell line

Project description:We demonstrate that AK4 down-regulation shRNAs significantly reduced cell migration and invasion in highly invasive lung cancer cell lines in vitro, as well as in lung metastases in vivo We used microarrays to analyze the AK4 regulated gene expression underlying invasion-metastasis cascade. CL1-0 lung adenocarcinoma cells with AK4 overexpression and CL1-5 cells with AK4 knockdown were selected for RNA extraction and hybridization on Affymetrix microarrays.

2012-12-03 | E-GEOD-37903 | biostudies-arrayexpress

Expression data from Chinese renal cell carcinoma cells with FSTL1 knocked down

Project description:Clear cell renal cell carcinoma (ccRCC), the major histotype of cancer derived from kidney, is lack of robust prognostic and/or predictive biomarker and powerful therapeutic target. We previously identified that follistatin-like protein 1 (FSTL1) was significantly down-regulated in ccRCC at the transcription level. In the present study, we characterized, for the first time, that FSTL1 immunostaining was selectively positive in the cytoplasm of distal convoluted tubules. The expression of FSTL1 was significantly lower in ccRCC tissues than in adjacent renal tissues (P<0.001), as measured using immunohistochemistry in 69 patients with paired specimens, and lower in most ccRCC cell lines than in human embryonic kidney cells, as measured by quantitative RT-PCR. Multivariate Cox regression analysis in 89 patients with follow-up data showed that FSTL1 expression in tumors conferred a favorable postoperative prognosis independently, with a hazard ratio of 0.325 (95% confidence interval: 0.118-0.894). FSTL1 knockdown promoted anchorage independent growth, mobility, and invasion of ccRCC cell lines and promoted cell cycle from G0/G1 phases into S phase; while over-expression of FSTL1 significantly attenuated cell migration ability in ACHN cells. FSTL1 knockdown resulted in decreased expression of E-cadherin and increased expression of N-cadherin in ccRCC cell lines significantly, indicating that FSTL1 may attenuate epithelial to mesenchymal transition in ccRCC. Microarray assay indicated that NF-ÎºB and HIF-2Î± pathways were activated following FSTL1 knockdown in ccRCC cells. Our study indicates that FSTL1 serves as a tumor suppressor in ccRCC, up-regulation of FSTL1 in cancer cells may be a candidate target therapy for advanced ccRCC. RNA samples were collected from NRCC-shsiscramble, NRCC-shFSTL1-1 and NRCC-shFSTL1-2 cells. Then samples were hybridized to Affymetrix arrays for mRNA profiling.

2016-01-20 | E-GEOD-76948 | biostudies-arrayexpress

Expression data from CL1-0 and CL1-5 lung cancer cell line.

2012-12-11 | GSE42407 | GEO

FSTL1 promotes cancer cell invasion through pro-invasive and pro-inflammatory pathways

Project description:This study identifies FSTL1 as a key component of tumor invasion in cutaneous squamous cell carcinoma

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Expression data from CL1-0 and CL1-5 lung cancer cell line.

Project description:A lung cancer cell model of invasive transformation was developed to select progressively invasive cell populations from a parental cell line of human lung adenocarcinoma, CL1. Five progressive sub-clones namely, CL1-1, CL1-2, CL1-3 CL1-4, and CL1-5 were selected using transwell and displayed increasing invasion potential (Chu et al, 1997). Here, we used microarrays to analyze and compare gene expression profiles between CL1-0 and CL1-5 for the identification of invasion/metastasis associated gene signatures. CL1-0 and CL1-5 lung cancer cell lines were used for RNA extraction and hybridization on Affymetrix microarrays. A total of 6 chips were used for microarray analysis including three biological repeats from CL1-0 and three biological repeats from CL1-5.

2012-12-11 | E-GEOD-42407 | biostudies-arrayexpress

FSTL1 promotes keratinocyte migration.

Project description:This study identifies FSTL1 as key component of intiating keratinocyte migration in skin Total RNA from N/TERT-1 keratinocytes transfected with a non-targeting siRNA or Smartpool siRNA against FSTL1 were subjected to microarray analysis

2013-03-02 | E-GEOD-41615 | biostudies-arrayexpress

Expression data from Chinese renal cell carcinoma cells with FSTL1 knocked down

Project description:Clear cell renal cell carcinoma (ccRCC), the major histotype of cancer derived from kidney, is lack of robust prognostic and/or predictive biomarker and powerful therapeutic target. We previously identified that follistatin-like protein 1 (FSTL1) was significantly down-regulated in ccRCC at the transcription level. In the present study, we characterized, for the first time, that FSTL1 immunostaining was selectively positive in the cytoplasm of distal convoluted tubules. The expression of FSTL1 was significantly lower in ccRCC tissues than in adjacent renal tissues (P<0.001), as measured using immunohistochemistry in 69 patients with paired specimens, and lower in most ccRCC cell lines than in human embryonic kidney cells, as measured by quantitative RT-PCR. Multivariate Cox regression analysis in 89 patients with follow-up data showed that FSTL1 expression in tumors conferred a favorable postoperative prognosis independently, with a hazard ratio of 0.325 (95% confidence interval: 0.118-0.894). FSTL1 knockdown promoted anchorage independent growth, mobility, and invasion of ccRCC cell lines and promoted cell cycle from G0/G1 phases into S phase; while over-expression of FSTL1 significantly attenuated cell migration ability in ACHN cells. FSTL1 knockdown resulted in decreased expression of E-cadherin and increased expression of N-cadherin in ccRCC cell lines significantly, indicating that FSTL1 may attenuate epithelial to mesenchymal transition in ccRCC. Microarray assay indicated that NF-κB and HIF-2α pathways were activated following FSTL1 knockdown in ccRCC cells. Our study indicates that FSTL1 serves as a tumor suppressor in ccRCC, up-regulation of FSTL1 in cancer cells may be a candidate target therapy for advanced ccRCC.

2016-01-20 | GSE76948 | GEO

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