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Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo.

ABSTRACT: Ninjurin 2 (NINJ2) is a novel adhesion molecule. Its expression and potential function in human colorectal cancer (CRC) cells are studied. We show that NINJ2 is overexpressed in established (HT-29) and primary CRC cells and in human colon cancer tissues. Its expression level is low in colon epithelial cells and normal colon tissues. NINJ2 shRNA or knockout (by CRSIPR/Cas9) potently inhibited human CRC cell survival and proliferation, while significantly inducing cell apoptosis. Conversely, lentivirus-mediated NINJ2 overexpression promoted CRC cell proliferation. NINJ2 co-immunoprecipitated with multiple RTKs (EGFR, PDGFR?/? and FGFR) in CRC cells and human colon cancer tissues. In HT-29 cells, RTKs' downstream signalings, Akt and Erk, were significantly inhibited by NINJ2 shRNA or knockout, but augmented following ectopic NINJ2 overexpression. In vivo, NINJ2-silenced or NINJ2-knockout CRC xenografts grew significantly slower than the control xenografts. Akt-Erk activation was largely inhibited in CRC xenografts with NINJ2 silencing or knockout. Taken together, NINJ2 overexpression promotes CRC cell growth in vitro and in vivo.

SUBMITTER: Li G

PROVIDER: S-EPMC6814613 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature

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Ninjurin 2 overexpression promotes human colorectal cancer cell growth <i>in vitro</i> and <i>in vivo</i>.

Li Gang G Zhou Li-Na LN Yang Han H He Xixi X Duan Yuxia Y Wu Fang F

Aging 20191009 19

Ninjurin 2 (NINJ2) is a novel adhesion molecule. Its expression and potential function in human colorectal cancer (CRC) cells are studied. We show that NINJ2 is overexpressed in established (HT-29) and primary CRC cells and in human colon cancer tissues. Its expression level is low in colon epithelial cells and normal colon tissues. NINJ2 shRNA or knockout (by CRSIPR/Cas9) potently inhibited human CRC cell survival and proliferation, while significantly inducing cell apoptosis. Conversely, lenti ...[more]

PMID: 31597121

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Project description:Background: Secreted protein acidic and rich in cysteine (SPARC) plays an important role in cancer development. The roles of SPARC in the liver hepatocellular carcinoma (LIHC) are unclear. Methods: GEPIA2 and UALCAN were used to analyze the SPARC mRNA expression levels in LIHC based on the TCGA database. The GEO database was used to verify the analysis results. Immunohistochemical (IHC) analysis was used to investigate the SPARC protein levels in LIHC tissues. The Kaplan-Meier (KM) plotter was used to analyze the correlation between SPARC and prognosis. The serum SPARC levels were measured by ELISA. CCK8 and murine xenograft models were used to investigate the effect of SPARC on the liver cancer growth in vitro and in vivo. SPARC-correlated genes were screened by LinkedOmics. Results: Based on the TCGA and GEO databases, the analysis showed that the SPARC mRNA expression levels were increased in tumor tissues and peripheral blood mononuclear cell (PBMC) from LIHC compared to normal controls. The IHC analysis showed an increased level of SPARC in LIHC tissues compared to adjacent non-tumor tissues. However, we found that the serum SPARC levels were lower in LIHC than those in healthy controls. The KM plotter showed that there was no significant correlation between the SPARC mRNA levels and overall survival. However, in sorafenib-treated LIHC patients, the high SPARC expression predicts favorable prognosis. Furthermore, the endogenous SPARC overexpression promotes liver cancer cell proliferation in vitro and tumor growth in vivo, while there was no significant effect of exogenous SPARC treatment on liver cancer cell proliferation. Function enrichment analysis of SPARC-correlated genes indicated a critical role of interaction with an extracellular matrix in SPARC-promoting cancer cell proliferation. Conclusion: SPARC mRNAs were increased in LIHC tumor tissues, and SPARC overexpression may promote the liver cancer growth. Further studies are needed to clarify the potential prognostic value of SPARC, both in tissues and in circulation.

Dataset Information

Ninjurin 2 overexpression promotes human colorectal cancer cell growth in vitro and in vivo.

Publications

Ninjurin 2 overexpression promotes human colorectal cancer cell growth <i>in vitro</i> and <i>in vivo</i>.

Similar Datasets

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