Alpha-2, 3-sialyltransferases regulate the multidrug resistance of chronic myeloid leukemia through miR-4701-5p targeting ST3GAL1

Li, Yan; Luo, Shihua; Dong, Wei; Song, Xianmin; Zhou, Huimin; Zhao, Lifen; Li, Jia

doi:10.1038/labinvest.2016.50

Cited by 22 publications

(14 citation statements)

References 28 publications

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“…Therefore, chemoresistance seems to reflect the level of ST3GAL1 expression in the different cell lines as it is doubtful that an untreated cell line could acquire resistance to cytotoxic drugs. A study on the role of α2,3-sialyltransferases on chemoresistance in chronic myeloid leukemia cell lines, also found that a multidrug-resistant phenotype was associated with the altered expression level of ST3GAL1 34 . Moreover, when the expression of ST3GAL1 was downregulated, sensitivity to adriamycin, paclitaxel, and vincristine increased.…”

Section: Discussionmentioning

confidence: 91%

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Sialyltransferase ST3GAL1 promotes cell migration, invasion, and TGF-β1-induced EMT and confers paclitaxel resistance in ovarian cancer

et al. 2018

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Sialyltransferases transfer sialic acid to nascent oligosaccharides and are upregulated in cancer. The inhibition of sialyltransferases is emerging as a potential strategy to prevent metastasis in several cancers, including ovarian cancer. ST3GAL1 is a sialyltransferase that catalyzes the transfer of sialic acid from cytidine monophosphate-sialic acid to galactose-containing substrates and is associated with cancer progression and chemoresistance. However, the function of ST3GAL1 in ovarian cancer is uncertain. Herein, we use qRT-PCR, western blotting, and immunohistochemistry to assess the expression of ST3GAL1 in ovarian cancer tissue and cell lines and investigate whether it influences resistance to paclitaxel in vitro and in a mouse xenograft model. We found that ST3GAL1 is upregulated in ovarian cancer tissues and in the ovarian cancer cell lines SKOV-3 and OVCAR3 but downregulated in A2780 ovarian cancer cells. Overexpression of ST3GAL1 in A2780 cells increases cell growth, migration, and invasion whereas ST3GAL1 knockdown in SKOV-3 cells decreases cell growth, migration, and invasion. Furthermore, overexpression of ST3GAL1 increases resistance to paclitaxel while downregulation of ST3GAL1 decreases resistance to paclitaxel in vitro, and overexpression of ST3GAL1 increases tumorigenicity and resistance to paclitaxel in vivo. Transforming growth factor-β1 can increase ST3GAL1 expression and induce ovarian cell epithelial–mesenchymal transition (EMT). However, knockdown of ST3GAL1 inhibits EMT expression. Taken together, our findings have identified a regulatory mechanism involving ST3GAL1 in ovarian cancer. ST3GAL1 may be a promising target for overcoming paclitaxel resistance in ovarian carcinoma.

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Section: Discussionmentioning

confidence: 91%

“…Human sialyltransferases are known to be upregulated in several cancers and are also associated with chemoresistance 32 – 34 . In the present study, we found that ST3GAL1 was upregulated in ovarian cancer tissues and ovarian cancer cell lines.…”

Section: Discussionmentioning

confidence: 99%

Sialyltransferase ST3GAL1 promotes cell migration, invasion, and TGF-β1-induced EMT and confers paclitaxel resistance in ovarian cancer

et al. 2018

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“…After data analyses, a total of 26 miRNAs, 248 mRNAs, 1118 lncRNAs, and 382 circRNAs were differential between miR‐145‐5p mimics and NC groups. We noted both tumor suppressive and oncogenic miRNAs were included in the differentially expressed miRNAs, among which miR‐148b‐3p, miR‐150‐3p, miR‐2116‐3p, miR‐3940‐5p, miR‐4653‐3p, miR‐4701‐5p, miR‐4741, miR‐4749‐3p, miR‐4769‐3p, and miR‐663a are tumor suppressive miRNAs . Moreover, miR‐1539, miR‐1825, miR‐3151‐3p, miR‐550a‐3p, miR‐550a‐5p, and miR‐575 are oncogenic miRNAs .…”

Section: Discussionmentioning

confidence: 95%

Identification of miR‐145‐5p‐Centered Competing Endogenous RNA Network in Laryngeal Squamous Cell Carcinoma

et al. 2019

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This study intends to investigate the transcriptional regulatory role of miR‐145‐5p in laryngeal squamous cell carcinoma (LSCC). LSCC cell line TU‐177 is transfected with miR‐145‐5p mimics, generating miR‐145‐5p‐overexpression LSCC cells. Whole transcriptome microarrays are used to investigate the differentially expressed lncRNAs, circRNAs, mRNAs, and miRNAs. The target genes of miRNAs are predicted and performed functional annotation. Additionally, the circRNAs, lncRNAs, and mRNAs that interact with miRNAs are predicted, and then the competing endogenous RNAs (ceRNAs) are predicted. Microarray analysis identifies 26 miRNAs, 248 mRNAs, 1118 lncRNAs, and 382 circRNAs differentially expressed in miR‐145‐5p overexpressed LSCC cells. Overall, 675 target genes are identified for the differentially expressed miRNAs, which involved in cell adhesion associated gene ontology (GO) terms, and MAPK and FoxO signaling pathways. The up‐regulated mRNAs involved in the pathway of ABC transporters, while the down‐regulated mRNAs involved in pathway of olfactory transduction. Moreover, 149 ceRNAs are predicted, which are associated with apoptosis, Wnt pathway, and metabolic pathway. Furthermore, qPCR results confirm that miR‐145‐5p affects expression of lncRNAs, miRNAs, mRNAs, and circRNAs in LSCC cells. Collectively, miR‑145‑5p may be inhibits LSCC progression via ceRNA‐mediated pathways, such as WNT2B‐miR‐145‐5p‐NONHSAT127539.2, CASP10‐miR‐145‐5p‐NONHSAT127539.2, CASP10‐miR‐145‐5p‐circ_0003519, and TPO‐miR‐145‐5p‐circ_0003519.

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“…High expression of ST3Gal1 is associated with advanced stage epithelial ovarian cancer (Wen et al, 2017). Altered levels of ST3GAL1 correspond to the drugresistant phenotype of chronic myeloid leukemia (CML) cell lines (Li et al, 2016). However, similar studies of the role of ST3Gal1 in RCC are rare.…”

Section: Discussionmentioning

confidence: 99%

The lncRNA MEG3 mediates renal cell cancer progression by regulating ST3Gal1 transcription and EGFR sialylation

Gong

Zhao

Pan

et al. 2020

Journal of Cell Science

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Long noncoding RNAs (lncRNAs) have emerged as important regulators of cancer progression. Abnormal sialylation leads to renal cell carcinoma (RCC) malignancy. However, the mechanism by which the lncRNA maternally expressed gene 3 (MEG3) mediates RCC progression by regulating ST3Gal1 transcription and EGFR sialylation is still unrevealed. Here, we found that the expression of MEG3 was higher in adjacent tissues than in RCC tissues, as well as downregulated in RCC cell lines compared to expression in normal renal cells. The proliferation, migration and invasion of RCC cells transfected with MEG3 was decreased, whereas knockdown of MEG3 had the opposite effect. The proliferative and metastatic abilities of RCC cells in vivo were concordant with their behavior in vitro. ST3Gal1 expression was dysregulated in RCC and was positively correlated with MEG3. By applying bioinformatics, c-Jun (also known as JUN) was identified as a transcription factor predicted to bind the promoter of ST3Gal1, and altered MEG3 levels resulted in changes to c-Jun expression. Furthermore, ST3Gal1 modulated EGFR sialylation to inhibit EGFR phosphorylation, which affected activation of the phosphoinositide 3-kinase (PI3K)–AKT pathway. Taken together, our findings provide a novel mechanism to elucidate the role of the MEG3–ST3Gal1–EGFR axis in RCC progression.

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Alpha-2, 3-sialyltransferases regulate the multidrug resistance of chronic myeloid leukemia through miR-4701-5p targeting ST3GAL1

Cited by 22 publications

References 28 publications

Sialyltransferase ST3GAL1 promotes cell migration, invasion, and TGF-β1-induced EMT and confers paclitaxel resistance in ovarian cancer

Sialyltransferase ST3GAL1 promotes cell migration, invasion, and TGF-β1-induced EMT and confers paclitaxel resistance in ovarian cancer

Identification of miR‐145‐5p‐Centered Competing Endogenous RNA Network in Laryngeal Squamous Cell Carcinoma

The lncRNA MEG3 mediates renal cell cancer progression by regulating ST3Gal1 transcription and EGFR sialylation

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