Glycomic alterations are associated with multidrug resistance in human leukemia

Zhang, Zhaohai; Zhao, Yongfu; Jiang, Lili; Xing, Miao; Zhou, Huimin; Li, Jia

doi:10.1016/j.biocel.2012.04.026

Cited by 42 publications

(32 citation statements)

References 35 publications

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“…Lattova et al (14) reported that N-glycomic changes in human breast carcinoma MCF-7 and T-lymphoblastoid cells occurred after treatment with herceptin and herceptin/Lipoplex. Our results also showed that glycomic alterations were associated with MDR in human leukemia (15). These studies have detected N-glycan alterations in resistant cancer cell line compared to its parent line, but systemic and complete information is still available on the correlation of N-glycans with drug resistance.…”

Section: Introductionsupporting

confidence: 66%

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

Xing

et al. 2013

IUBMB Life

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Drug resistance is a major problem in cancer chemotherapy. Aberrant glycosylation has been known to be associated with cancer chemoresistance. Aim of this work is to investigate the alterations of glycogene and N-glycan involved in multidrug resistance (MDR) in human breast cancer cell lines. Using real-time polymerase chain reaction (PCR) for quantification of glycogenes, fluorescein isothiocyanate (FITC)-lectin binding for glycan profiling, and mass spectrometry for N-glycan composition, the expression of glycogenes, glycan profiling, and N-glycan composition differed between drug-resistant MCF/ ADR cells and the parental MCF-7 line. Further analysis of the N-glycan regulation by tunicamycin (TM) application or PNGase F treatment in MCF/ADR cells showed partial inhibition of the N-glycan biosynthesis and increased sensitivity to chemotherapeutic drugs dramatically both in vitro and in vivo. Using an RNA interference strategy, we showed that the downregulation of MGAT5 in MCF/ADR cells could enhance the chemosensitivity to antitumor drugs both in vitro and in vivo. Conversely, a stable high expression of MGAT5 in MCF-7 cells could increase resistance to chemotherapeutic drugs both in vitro and in vivo. In conclusion, the alterations of glycogene and N-glycan in human breast cancer cells correlate with tumor sensitivity to chemotherapeutic drug and have significant implications for the development of new treatment strategies. V C 2013 IUBMB Life, 65(5): 409-422, 2013.

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Section: Introductionsupporting

confidence: 66%

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

Xing

et al. 2013

IUBMB Life

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“…Structures containing a bisecting glcnac were found to be decreased in the colorectal tumor, whereas sulfated glycans, paucimannosidic glycans, and glycans containing a sialylated lewis type epitope were shown to be increased in tumor tissues (23). rencently, aberrant changes in n-glycans have been shown to be associated with drug resistance (9,24). Swainsonine, an inhibitor of n-glycan biosynthesis, could reduce 5-fu tolerance in the multistage resistance of crc cells (12).…”

Section: Discussionmentioning

confidence: 99%

“…n-glycans are also related to tumor progression and metastasis as well as to immune system activity, and their potential relationship to chemoresistance has recently been examined (8). Zhang et al showed that n-glycomic alterations were associated with adriamycin resistance in human leukemia (9). increased levels and defective n-glycosylation of multidrug resistance-associated proteins (MrPs) in ovarian carcinoma cells resistant to oxaliplatin have also been reported (10).…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of β3GnT8 reverses 5-fluorouracil resistance in human colorectal cancer cells via inhibition the biosynthesis of polylactosamine-type N-glycans

Shen

et al. 2014

International Journal of Oncology

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Abstract. aber rant glycosylation is known to be associated with cancer chemoresistance. β-1,3-n-acetylglucosaminyltransferase (β3gnt)8, which synthesizes polylactosamine on β1-6 branched n-glycans, is dramatically upregulated in colorectal cancer (crc). 5-fluorouracil (5-fu) resistance remains a major obstacle to the chemotherapy of crc. However, little is known with regard to the correlation between 5-fu resistance and the expression of β3gnt8 in crc. in this study, a 5-fu-resistant cell line (SW620/5-fu) was generated, and 50% inhibition concentration (ic50) of 5-fu was determined by Mtt assay. flow cytometry and lectin blot analysis were performed to detect the alteration of polylactosamine structures. Quantitative rt-Pcr and western blot analysis were used to identify and evaluate candidate genes involved in the synthesis of polylactosamine in SW620/5-fu cells. We found polylactosamine chains were significantly increased in SW620/5-fu cells. inhibition of the biosynthesis of polylactosamine by 3'-azidothymidine (aZt) was able to reduce 5-fu tolerance. further studies showed that β3gnt8 expression was also upregulated in 5-fu-resistant cancer cells, and knockdown of β3gnt8 by rna interference reversed 5-fu resistance through, at least partly, by suppressing the formation of polylactosamine. in conclusion, the alteration of β3gnt8 in crc cells correlates with tumor sensitivity to the chemotherapeutic drug and has significant implication for the development of new treatment strategies.

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“…The changes of glycans attached on cell glycoproteins have been linked to drug resistance in leukemia. 3,4 Therefore, much attention has been paid on regulation of glycosyltransferases in an effort to overcome MDR in the treatment of CML.…”

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confidence: 99%

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

Luo

Dong

et al. 2016

Laboratory Investigation

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The aberrant sialylation profile on the surface of leukemia cells has been recognized for its potential diagnostic value towards assessing leukemia multidrug resistance (MDR). MicroRNAs as endogenous regulators of gene expression have been implicated in treating MDR. In this study, we describe the differential expressional profiles of α-2, 3-sialyltransferases (ST) and miR-4701-5p in three pairs of chronic myeloid leukemia (CML) cell lines and 48 clinical samples of bone marrow mononuclear cells from CML patients. The altered expression level of ST3GAL1 was found corresponding to the drugresistant phenotype (with and without adriamycin resistance) of CML cell lines both in vitro and in vivo. Further the results showed that miR-4701-5p directly targeted ST3GAL1 to reduce CML cells resistance to multiple chemotherapeutics in vitro and to convert tumor cells from adriamycin resistant to susceptible in vivo of mice. These results indicate that differential expression of α-2,3 ST is involved in MDR of CML, and that miR-4701-5p regulates the susceptibility of CML cells to multiple drugs, at least in part, through targeting ST3GAL1.

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Glycomic alterations are associated with multidrug resistance in human leukemia

Cited by 42 publications

References 35 publications

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

Functional roles of glycogene and N‐glycan in multidrug resistance of human breast cancer cells

Knockdown of β3GnT8 reverses 5-fluorouracil resistance in human colorectal cancer cells via inhibition the biosynthesis of polylactosamine-type N-glycans

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

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