Overexpression of CAP1 and its significance in tumor cell proliferation, migration and invasion in glioma

Fan, Yi‐Ming; Cui, Chenchen; Yunfen, Zhu; Zhang, Lei; Shi, Meng; Yu, Jiwei; Bai, Jing; Zheng, Junnian

doi:10.3892/or.2016.4936

Cited by 15 publications

(12 citation statements)

References 31 publications

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“…CAP1 is involved in the cyclic AMP pathway and interacts with the actin cytoskeleton influencing cell adhesion [ 82 ]. CAP1 expression has been reported to be positively correlated with proliferation, migration, invasion, and WHO grade of gliomas [ 3 , 21 ].…”

Section: Resultsmentioning

confidence: 99%

Network-based analysis of oligodendrogliomas predicts novel cancer gene candidates within the region of the 1p/19q co-deletion

Gladitz

Klink

Seifert

2018

acta neuropathol commun

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Oligodendrogliomas are primary human brain tumors with a characteristic 1p/19q co-deletion of important prognostic relevance, but little is known about the pathology of this chromosomal mutation. We developed a network-based approach to identify novel cancer gene candidates in the region of the 1p/19q co-deletion. Gene regulatory networks were learned from gene expression and copy number data of 178 oligodendrogliomas and further used to quantify putative impacts of differentially expressed genes of the 1p/19q region on cancer-relevant pathways. We predicted 8 genes with strong impact on signaling pathways and 14 genes with strong impact on metabolic pathways widespread across the region of the 1p/19 co-deletion. Many of these candidates (e.g. ELTD1, SDHB, SEPW1, SLC17A7, SZRD1, THAP3, ZBTB17) are likely to push, whereas others (e.g. CAP1, HBXIP, KLK6, PARK7, PTAFR) might counteract oligodendroglioma development. For example, ELTD1, a functionally validated glioblastoma oncogene located on 1p, was overexpressed. Further, the known glioblastoma tumor suppressor SLC17A7 located on 19q was underexpressed. Moreover, known epigenetic alterations triggered by mutated SDHB in paragangliomas suggest that underexpressed SDHB in oligodendrogliomas may support and possibly enhance the epigenetic reprogramming induced by the IDH-mutation. We further analyzed rarely observed deletions and duplications of chromosomal arms within oligodendroglioma subcohorts identifying putative oncogenes and tumor suppressors that possibly influence the development of oligodendroglioma subgroups. Our in-depth computational study contributes to a better understanding of the pathology of the 1p/19q co-deletion and other chromosomal arm mutations. This might open opportunities for functional validations and new therapeutic strategies.Electronic supplementary materialThe online version of this article (10.1186/s40478-018-0544-y) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Network-based analysis of oligodendrogliomas predicts novel cancer gene candidates within the region of the 1p/19q co-deletion

Gladitz

Klink

Seifert

2018

acta neuropathol commun

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“…In addition, co‐localization of CAP1, CYPB, KDELR2, and EB1 with FAM134B, further strengthen their physical interactions in colon cancer cells. It was noted that these proteins regulate multiple processes (eg, cell proliferation, migration, invasion, and metastasis) involved in the carcinogenesis of different types of cancers . Therefore, interactions with this cancer growth‐related proteins and increased growth and proliferation of cancer cells followed by FAM134B suppression implies that FAM134B might play a crucial role in the pathogenesis of cancer.…”

Section: Discussionmentioning

confidence: 99%

Protein interactions of FAM134B with EB1 and APC/beta‐catenin in vitro in colon carcinoma

Islam

Chaousis

Wahab

et al. 2018

Molecular Carcinogenesis

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FAM134B is an autophagy regulator of endoplasmic reticulum and acts as a cancer suppressor in colon cancer. However, the molecular signaling pathways by which FAM134B interacts within colon carcinogenesis is still unknown. Herein, this study aims to determine the interacting partners of FAM134B for the first time in colon cancer and to explore the precise location of FAM134B in cancer signalling pathways. Liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS) followed by anti-FAM134B co-immune precipitation of FAM134B interacting complex was used to identify the potential interactors of FAM134B in colon cancer cells. Western blot and confocal microscopic analysis were used to validate the physical interactions of FAM134B with the interactors. Lentiviral shRNA mediated silencing of FAM134B was used to examine the modulation of FAM134B interactors in cells. We have identified 29 novel binding partners, including CAP1, RPS28, FTH1, KDELR2, MAP4, EB1, PSMD6, PPIB/CYPB etc. Subsequent immunoassays confirmed the direct physical interactions of FAM134B with CAP1, EB1, CYPB, and KDELR2 in colon cancer cells. Exogenous suppression of FAM134B has led to significant upregulation of EB1 as well as reduction of KDELR2 expression. It was noted that overexpression of EB1 promotes WNT/β-catenin signaling pathways via inactivating tumor suppressor APC followed by activating β-catenin in colorectal carcinogenesis. This study has first time reported the gene signaling networks with which FAM134B interacts and noted that FAM134B is involved in the regulation of WNT/β-catenin pathway by EB1-mediated modulating of APC in colon cancer cells.

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“…Glioma cells are highly invasiveness and infiltrative multiple brain regions (20)(21)(22)(23). Targeting specific tumor-promoting genes may provide a promising alternative treatment to the current standards (24). Collagen is a biological macromolecular protein synthetized and widely present in animal cells, which content and sort is various.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of collagen α‑1(III) inhibits glioma cell proliferation and migration and is regulated by miR128‑3p

et al. 2018

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As a member of the collagen family, collagen α-1(III) (COL3A1) is an important protein in the development and progression of several tumors. However, the role of COL3A1 in glioma is not yet clear. The present study examined the expression and function of COL3A1 in glioma cell behavior and identified microRNA (miRNA) regulators. It was demonstrated that COL3A1 expression was upregulated in glioma and directly correlated with the tumor grade. Analysis of the GSE4290 and GSE7696 profiles acquired from the Gene Expression Omnibus database also revealed an increased COL3A1 expression in malignant gliomas compared with the lower grade gliomas and non-tumor brain tissue, which was directly correlated with glioma grade. To explore the functional role of COL3A1 in glioma cell growth, small interfering RNA interference was applied to inhibit COL3A1 expression in Hs683 and U251 cells. The relative COL3A1 mRNA and protein expression levels were significantly reduced in the knockdown cells as determined by western blot analysis. In addition, decreased COL3A1 expression in Hs683 and U251 glioma cells resulted in a delay in cell growth and colony disruption as determined by MTS and colony formation assays. Wound healing analysis indicated that cells with suppressed expression of COL3A1 had a reduced ability to migrate. COL3A1 mRNA levels were inversely correlated with the miR128-3p level in glioma, suggesting that miR128-3p expression is associated with COL3A1 inhibition as verified by reverse transcription-quantified polymerase chain reaction. These results suggest that COL3A1 may be a novel regulator of glioblastoma cell behavior and may represent a novel target for gene therapies against glioma.

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Overexpression of CAP1 and its significance in tumor cell proliferation, migration and invasion in glioma

Cited by 15 publications

References 31 publications

Network-based analysis of oligodendrogliomas predicts novel cancer gene candidates within the region of the 1p/19q co-deletion

Network-based analysis of oligodendrogliomas predicts novel cancer gene candidates within the region of the 1p/19q co-deletion

Protein interactions of FAM134B with EB1 and APC/beta‐catenin in vitro in colon carcinoma

Knockdown of collagen α‑1(III) inhibits glioma cell proliferation and migration and is regulated by miR128‑3p

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