Increased fucosylation has a pivotal role in multidrug resistance of breast cancer cells through miR-224-3p targeting FUT4

Feng, Xueping; Zhao, Lifen; Gao, Shuhang; Song, Xianmin; Dong, Wei; Zhao, Yongfu; Zhou, Huimin; Cheng, Lei; Miao, Xudong; Li, Jia

doi:10.1016/j.gene.2015.12.028

Cited by 49 publications

(37 citation statements)

References 33 publications

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“…Recently, our data also showed FUT4 was crucial regulators of cancer response to chemotherapy in breast cancer and hepatocellular carcinoma, as well as of invasiveness and tumorigenicity in breast cancer. 27, 29, 30 Thus, miR-26a/26b-induced FUT4 provided a conserved mechanism for the suppressive role of miR-26a/26b during aggressiveness of CRC.…”

Section: Discussionmentioning

confidence: 98%

“…28 FUT4 was found as a novel direct target of miR-224-3p, and the association of FUT4 expression with miR-224-3p was validated in breast cancer mouse models and cell lines. 29 Furthermore, miR-493-5p directly targeted and inhibited FUT4 expression in breast cancer. 30 In the current study, in silico prediction has identified miR-26a and miR-26a targeting FUT4 in CRC cells, and forced expression of miR-26a and miR-26a phenocopied the effects of FUT4 depletion in CRC cell lines, supporting a role of the two miRNAs in regulating FUT4 expression in CRC.…”

Section: Discussionmentioning

confidence: 99%

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Tumor-suppressive miR-26a and miR-26b inhibit cell aggressiveness by regulating FUT4 in colorectal cancer

Sun

Liu

et al. 2017

Cell Death Dis

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Metastasis is a multistep molecular network process, which is the major cause of death in patients with colorectal cancer (CRC). MicroRNAs (miRNAs) play pivotal roles in tumorigenesis as either tumor suppressors or oncogenes. Increased expression of fucosyltransferase4 (FUT4) has been reported to be associated with the invasive and metastatic properties of CRC. Here to identify potential key miRNAs and their target genes for colorectal cancer (CRC), we compared miRNA expression profiles between metastatic CRC cell SW620 and primary CRC cell SW480. Microarray analysis revealed that there were 85 differentially expressed miRNAs in SW620 cells with highly metastatic potential compared to SW480 cells with lowly metastatic potential. The expression of miR-26a and miR-26b were lower in SW620 cells than in SW480 cells, as well as downregulated in tumor tissues than in adjacent normal tissues of CRC patients. By applying bioinformatic approaches for the prediction of miRNA targeting 3′-UTR of FUT4, we identified FUT4 as one of the miR-26a/26b-targeted genes, while the expression of the target gene exhibited patterns opposite to that of miR-26a/26b in CRC cell lines, tumor tissues and corresponding adjacent tissues. Forced miR-26a/26b expression affected migratory behavior of CRC cells and FUT4 expression, while altered expression of FUT4 in CRC cell lines modulated progression upon transfection with miR-26a/26b mimic or inhibiter. FUT4 also regulated directly aggressiveness of SW620 and SW480 cells. Moreover, statistical analyses revealed that low miR-26a/26b levels and high expression of FUT4 were positively correlated with poor overall survival. The identified CRC-restricted miR-26a and miR-26b might be implicated in cancer progression via their target gene FUT4, suggesting their potential usage in CRC treatment.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Tumor-suppressive miR-26a and miR-26b inhibit cell aggressiveness by regulating FUT4 in colorectal cancer

Sun

Liu

et al. 2017

Cell Death Dis

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“…34 Our recent results also showed that miR-224-3p directly targeted 3′-UTR of fucosyltransferase FUT4 mRNA and sensitized drug-resistant breast cancer cells to chemotherapeutics and reduced the growth rate of breast cancer xenografts in vivo . 35 …”

Section: Discussionmentioning

confidence: 99%

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

Dong

et al. 2016

Cell Death Dis

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Sialylation is one of the altered glycosylation patterns associated with cancer progression. In this study, we investigated the N-glycan profiles of breast cancer patients and cell lines to reveal sialylation associated with breast cancer progression, and provided new evidences of miRNA-mediated sialylation. MALDI-TOF MS analysis revealed that N-glycans found in breast cancer tissues and breast cancer cell MDA-MB-231 featured increased levels of sialylation compared with adjacent tissues and normal breast epithelial cell MCF-10A. The expressional profiles of 20 sialyltransferase genes were then analyzed and found significantly different comparing breast cancer samples with adjacent tissues, and two breast cancer cell lines MDA-MB-231 and MCF-7 with different metastatic potential and MCF-10A cells. Tumor tissues and highly metastatic breast cancer cell line MDA-MB-231 exhibited higher levels of ST8SIA4. Knocking down ST8SIA4 in breast cancer cell lines significantly inhibited their malignant behaviors including cell proliferation and invasion in a sialyltransferase-dependent manner. By applying bioinformatic approaches for the prediction of miRNA targeting 3′-UTR of ST8SIA4, we identified ST8SIA4 as one of the miR-26a/26b-targeted genes. Further data analysis revealed the inversely related expression of ST8SIA4 and miR-26a/26b in breast cancer cells, tumor tissues and corresponding adjacent tissues. The ability of miR-26a/26b to interact specifically with and regulate the 3′-UTR of ST8SIA4 was demonstrated via a luciferase reporter assay. The forced expression of miR-26a/26b was able to induce a decrease of ST8SIA4 level and also to affect breast cancer cells progression, while altered expression of ST8SIA4 in breast cancer cells modulated progression upon transfection with miR-26a/26b mimics or inhibiter. Taken together, these results indicate that changes in the glycosylation patterns and sialylation levels may be useful markers of the progression of breast cancer, as well as miR-26a/26b may be widely involved in the regulation of sialylation machinery by targeting ST8SIA4.

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“…In a screen to identify dysregulated miRNAs in Her2-positive breast cancers, miR-146a was found to be up-regulated whereas miR-181d and miR-195 were down-regulated (Tashkandi et al , 2015). MiR-224 was reported to play a pivotal role in multidrug resistance of breast cancer cells by targeting FUT4 (Feng et al, 2015). MiR-27a was found to regulate the sensitivity of breast cancer cells to cisplatin treatment .…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer

Zhu

Wang

Zhu

et al. 2016

Biological Chemistry

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Triple negative breast cancer lacking estrogen receptor (ER), progesterone receptor and Her2 account for account for the majority of the breast cancer deaths, due to the lack of specific gene targeted therapy. Our current study aimed to investigate the role of miR-544 in triple negative breast cancer. Endogenous levels of miR-544 were significantly lower in breast cancer cell lines than in human breast non-tumorigenic and mammary epithelial cell lines. We found that miR-544 directly targeted the 3'-untranslated region (UTR) on both Bcl6 and Stat3 mRNAs, and overexpression of miR-544 in triple negative breast cancer cells significantly down-regulated expressions of Bcl6 and Stat3, which in turn severely inhibited cancer cell proliferation, migration and invasion in vitro. Employing a mouse xenograft model to examine the in vivo function of miR-544, we found that expression of miR-544 significantly repressed the growth of xenograft tumors. Our current study reported miR-544 as a tumor-suppressor microRNA particularly in triple negative breast cancer. Our data supported the role of miR-544 as a potential biomarker in developing gene targeted therapies in the clinical treatment of triple negative breast cancer.

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Increased fucosylation has a pivotal role in multidrug resistance of breast cancer cells through miR-224-3p targeting FUT4

Cited by 49 publications

References 33 publications

Tumor-suppressive miR-26a and miR-26b inhibit cell aggressiveness by regulating FUT4 in colorectal cancer

Tumor-suppressive miR-26a and miR-26b inhibit cell aggressiveness by regulating FUT4 in colorectal cancer

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

MicroRNA-544 down-regulates both Bcl6 and Stat3 to inhibit tumor growth of human triple negative breast cancer

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