CARMA3 is overexpressed in human glioma and promotes cell invasion through MMP9 regulation in A172 cell line

Feng, Xingjun; Miao, Guozhuan; Han, Yipeng; Xu, Yong

doi:10.1007/s13277-013-1018-2

Cited by 19 publications

(7 citation statements)

References 23 publications

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“…Matrix metalloproteases (MMPs) are important in tumor growth, invasion and metastasis (15). Studies have shown that matrix metallopeptidase 9 (MMP-9), one of the most important MMPs, functioned in the migration, invasion and metastasis of numerous types of cancer, including CRC, through various signaling pathways (16)(17)(18)(19)(20)(21)(22)(23). MMP-9, activated by astrocyte elevated gene-1 (24), ERK-dependent induced MMP-9 (25) and the p38-MMP-9 pathway (26), increases the invasiveness of CRC.…”

Section: Introductionmentioning

confidence: 99%

B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer

Liu

Zhang

Zou

et al. 2015

Molecular Medicine Reports

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B7‑H3, a newly identified co‑stimulatory molecule, has been reported to be highly expressed in a number of types of cancer and is associated with a poor prognosis. Transwell experiments and a wound-healing assay were used to detect the role of over‑expressed B7‑H3 on cell migration and invasion in colorectal cancer (CRC) cells. The expression level of matrix metallopeptidase 9 (MMP‑9) was further investigated by zymography experiments and western blot analysis, and involvement of the Janus kinase 2 (Jak2) signal transducer and activator of transcription 3 (STAT3) signaling pathway was determined using AG490, a Jak2 selective inhibitor. Data showed that overexpression of B7‑H3 promoted cell migration and invasion in CRC. Further investigation certified that enhanced expression of B7‑H3 elevated MMP‑9 through upregulation of the Jak2‑Stat3 signaling pathway. Due to its pro‑migratory and pro‑invasive function, B7‑H3 may serve as a therapeutic target in the treatment of CRC.

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Section: Introductionmentioning

confidence: 99%

B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer

Liu

Zhang

Zou

et al. 2015

Molecular Medicine Reports

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“…MMP-9 mRNA expression was found to correlate with colorectal cancer cell invasion, indicating that the inhibitory effect of miR-195 on colorectal cancer cell invasion may at least partially be mediated through the downregulation of MMP-9, by directly targeting CARMA3. In accordance with these findings, Feng et al (15) reported that CARMA3 promoted glioma cell invasion through upregulating the expression of MMP-9.…”

Section: Discussionmentioning

confidence: 56%

“…Recently, Feng et al (15) reported that CARMA3 promoted glioma cell invasion through MMP-9, a key tumor invasion factor. Thus, to investigate the mechanism by which miR-195 regulates colorectal cancer cell invasion, MMP-9 mRNA expression was assessed in each group.…”

Section: Mir-195 Inhibits Colorectal Cancer Cell Invasion Through Tarmentioning

confidence: 99%

MicroRNA-195 inhibits colorectal cancer cell proliferation, colony-formation and invasion through targeting CARMA3

Wang

Liu

et al. 2014

Molecular Medicine Reports

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MicroRNA (miR)‑195 has been reported to be a tumor suppressor. Downregulation of miR‑195 has been shown to correlate with lymph node metastasis and poor prognosis in colorectal cancer. However, the specific regulatory role of miR‑195 in colorectal cancer cells is yet to be elucidated. In the present study, miR‑195 expression was significantly reduced in colorectal cancer tissues. Furthermore, CARMA3 was identified as a novel target of miR‑195, which was observed to be upregulated in colorectal cancer. In addition, downregulation of miR‑195 increased CARMA3 protein expression, whereas miR‑195 upregulation suppressed CARMA3 protein expression in SW480 and HT29 colorectal cancer cells. Moreover, overexpression of miR‑195 downregulated cell proliferation, colony‑formation and invasion in SW480 and HT29 cells, which was reversed upon CARMA3 overexpression. In conclusion, the findings of the present study suggest that miR‑195 has a suppressive role in colorectal cancer cells through directly targeting CARMA3. Therefore, CARMA3 may be a potential target for the treatment of colorectal cancer.

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“…Furthermore, CARMA3 knockdown in breast cancer cells with high endogenous CARMA3 resulted in increased paclitaxel-induced apoptosis, while overexpression of CARMA3 resulted in enhanced proliferation and reduced apoptosis, results which suggested a role for CARMA3 in chemotherapeutic resistance ( 124 ). In glioma patient tumor specimens, 26% of samples showed CARMA3 overexpression relative to normal astrocytes in the same specimen ( 125 ); the authors also showed that CARMA3 knockdown in a glioma cell line suppresses cell invasion in vitro and results in decreased expression of MMP9, a matrix metalloprotease closely linked with tissue invasion. These results suggested a possible mechanism by which C3BM signaling promotes invasion in human glioma.…”

Section: Other Studies Of Carma3 In Solid Tumorsmentioning

confidence: 99%

CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis

et al. 2018

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The CARMA–Bcl10–MALT1 (CBM) signalosome is an intracellular protein complex composed of a CARMA scaffolding protein, the Bcl10 linker protein, and the MALT1 protease. This complex was first recognized because the genes encoding its components are targeted by mutation and chromosomal translocation in lymphoid malignancy. We now know that the CBM signalosome plays a critical role in normal lymphocyte function by mediating antigen receptor-dependent activation of the pro-inflammatory, pro-survival NF-κB transcription factor, and that deregulation of this signaling complex promotes B-cell lymphomagenesis. More recently, we and others have demonstrated that a CBM signalosome also operates in cells outside of the immune system, including in several solid tumors. While CARMA1 (also referred to as CARD11) is expressed primarily within lymphoid tissues, the related scaffolding protein, CARMA3 (CARD10), is more widely expressed and participates in a CARMA3-containing CBM complex in a variety of cell types. The CARMA3-containing CBM complex operates downstream of specific G protein-coupled receptors (GPCRs) and/or growth factor receptor tyrosine kinases (RTKs). Since inappropriate expression and activation of GPCRs and/or RTKs underlies the pathogenesis of several solid tumors, there is now great interest in elucidating the contribution of CARMA3-mediated cellular signaling in these malignancies. Here, we summarize the key discoveries leading to our current understanding of the role of CARMA3 in solid tumor biology and highlight the current gaps in our knowledge.

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CARMA3 is overexpressed in human glioma and promotes cell invasion through MMP9 regulation in A172 cell line

Cited by 19 publications

References 23 publications

B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer

B7-H3 promotes cell migration and invasion through the Jak2/Stat3/MMP9 signaling pathway in colorectal cancer

MicroRNA-195 inhibits colorectal cancer cell proliferation, colony-formation and invasion through targeting CARMA3

CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis

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