Potential of tumor-suppressive miR-596 targeting LGALS3BP as a therapeutic agent in oral cancer

Endo, Hironori; Muramatsu, Tomoki; Furuta, Mayuko; Uzawa, Narikazu; Pimkhaokham, Atiphan; Amagasa, Teruo; Inazawa, Johji; Kozaki, Ken Ichi

doi:10.1093/carcin/bgs376

Cited by 61 publications

(40 citation statements)

References 36 publications

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“…High serum or tissue level of LGALS3BP has been confirmed to be associated with various malignant tumor, like breast cancer and metastasis [9]. By using immunohistochemistry and western blotting, we confirmed LGALS3BP was up regulated in ovarian cancer (Figure 2, 3 and Supplementary Figure S2), which was consistent with our quantitative proteomics results (Supplementary Figure S1) and previous reports [10].…”

Section: Discussionsupporting

confidence: 91%

Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics

Chen

Cao

et al. 2016

Oncotarget

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Ovarian cancer is the most lethal gynecological malignant tumor because of its high recurrence rate. In the present work, in order to find new therapeutic targets, we identified 8480 proteins in thirteen pairs of ovarian cancer tissues and normal ovary tissues through quantitative proteomics. 498 proteins were found to be differentially expressed in ovarian cancer, which involved in various cellular processes, including metabolism, response to stimulus and biosynthetic process. The expression levels of chloride intracellular channel protein 1 (CLIC1) and lectin galactoside-binding soluble 3 binding protein (LGALS3BP) in epithelial ovarian cancer tissues were significantly higher than those in normal ovary tissues as confirmed by western blotting and immunohistochemistry. The knockdown of CLIC1 in A2780 cell line downregulated expression of CTPS1, leading to the decrease of CTP and an arrest of cell cycle G1 phase, which results into a slower proliferation. CLIC1-knockdown can also slow down the tumor growth in vivo. Besides, CLIC1-knockdown cells showed an increased sensitivity to hydrogen peroxide and cisplatin, suggesting that CLIC1 was involved in regulation of redox and drug resistance in ovarian cancer cells. These results indicate CLIC1 promotes tumorgenesis, and is a potential therapeutic target in epithelial ovarian cancer treatment.

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Section: Discussionsupporting

confidence: 91%

Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics

Chen

Cao

et al. 2016

Oncotarget

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“…Using primers which encompass all known or predicted transcript variants (90), LGALS3BP cDNA was amplified via PCR and sequenced. The sequence encoded the four LGALS3BP peptides detected by mass spectrometry, and was identical to human LGALS3BP from oral squamous carcinoma cells (93), and is identical to the sequence of the recombinant full-length human LGALS3BP (R&D datasheet).…”

Section: Resultsmentioning

confidence: 99%

Galectin-3 Binding Protein Secreted by Breast Cancer Cells Inhibits Monocyte-Derived Fibrocyte Differentiation

White

Roife

Gomer

2015

The Journal of Immunology

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To metastasize, tumor cells often need to migrate through a layer of collagen-containing scar tissue which encapsulates the tumor. A key component of scar tissue and fibrosing diseases is the monocyte-derived fibrocyte, a collagen-secreting pro-fibrotic cell. To test the hypothesis that invasive tumor cells may block the formation of the fibrous sheath, we determined if tumor cells secrete factors that inhibit monocyte-derived fibrocyte differentiation. We found that the human metastatic breast cancer cell line MDA-MB 231 secretes activity that inhibits human monocyte-derived fibrocyte differentiation, while less aggressive breast cancer cell lines secrete less of this activity. Purification indicated that Galectin-3 Binding Protein (LGALS3BP) is the active factor. Recombinant LGALS3BP inhibits monocyte-derived fibrocyte differentiation, and immunodepletion of LGALS3BP from MDA-MB 231 conditioned media removes the monocyte-derived fibrocyte differentiation-inhibiting activity. LGALS3BP inhibits the differentiation of monocyte-derived fibrocytes from wild-type mouse spleen cells, but not from SIGN-R1−/− mouse spleen cells, suggesting that CD209/SIGN-R1 is required for the LGALS3BP effect. Galectin-3 and galectin-1, binding partners of LGALS3BP, potentiate monocyte-derived fibrocyte differentiation. In breast cancer biopsies, increased levels of tumor cell-associated LGALS3BP were observed in regions of the tumor that were invading the surrounding stroma. These findings suggest LGALS3BP and galectin-3 as new targets to treat metastatic cancer and fibrosing diseases.

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“…1A–B, S1A–B) located in the 5′-flanking regions, which play important roles on regulating gene expression. Among these loci, the expression of seven ( miR-130b , miR-132 , miR-191 , miR-212 , miR-335 , miR-363 and miR-596 ) has been previously reported to be associated with cancer development and/or regulated by DNA methylation [8–13]. All 13 miRNA loci were evaluated by COBRA in six endometrial cancer cell lines (AN3CA, Ishikawa, HEC1A, KLE, RL95-2, and SK-UT-1B, Fig.…”

Section: Resultsmentioning

confidence: 99%

Hypermethylation of miR-203 in endometrial carcinomas

Huang¹,

Kuo²,

Chen³

et al. 2014

Gynecologic Oncology

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Objectives Aberrant expression of SOX4 in endometrial cancer has been identified and partially was contributed to hypermethylation of miR-129-2. Other miRNAs are suspected to influence SOX 4 as well. The current study seeks to identify other hypermethylated miRNAs that regulate SOX4 in endometrial carcinomas. Methods Methylation levels of miRNA promoter regions were measured by combined bisulfite restriction analysis (COBRA) and pyrosequencing assays. Gene expression was determined by RT-qPCR. Methylation level of a miRNA locus was corrected with clinicopathologic factors for 252 gynecological specimens. Results In silico analysis identified 13 miRNA loci bound on the 3′-UTR of SOX4. Using COBRA assays, increased methylation of miR-203, miR-219-2, miR-596, and miR-618 was detected in endometrial cancer cells relative to those seen in a normal cell line and in normal endometrium. Transfection of a miR-203 mimic decreased SOX4 gene expression. Hypermethylation of miR-203 was detected in 52% of type I endometrioid endometrial carcinomas (n=131) but was not seen in any of 10 uninvolved normal endometria (P<0.001). Methylation status of miR-203 was significantly associated with microsatellite instability and MLH1 methylation in endometrial tumors (P<0.001). Furthermore, hypermethylation of miR-203 was found in endometrioid and clear endometrial subtype tumors, but not in cervical squamous cell and ovarian carcinomas. Conclusions Hypermethylation of miR-203 is a frequent event in endometrial carcinomas and is strongly associated with microsatellite instability and MLH1 methylation status. Thus, miR-203 methylation level might represent a marker for patients with endometrioid and clear endometrial sub-cancers.

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Potential of tumor-suppressive miR-596 targeting LGALS3BP as a therapeutic agent in oral cancer

Cited by 61 publications

References 36 publications

Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics

Identification and validation of differentially expressed proteins in epithelial ovarian cancers using quantitative proteomics

Galectin-3 Binding Protein Secreted by Breast Cancer Cells Inhibits Monocyte-Derived Fibrocyte Differentiation

Hypermethylation of miR-203 in endometrial carcinomas

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