Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

Zhang, Xiaopeng; Pan, Chensheng; Zhou, Lei; Cai, Zhaogen; Zhao, Shufang; Yu, Dihua

doi:10.1186/s12885-016-2981-y

Cited by 26 publications

(26 citation statements)

References 46 publications

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“…This could be explained by two reasons: (a) What is often described as “normal tissue adjacent to tumor tissue” in oral cancer is frequently not the case as there is very close proximity of the normal tissue to the tumor part; and (b) The normal tissue taken into the study may have a population of cells with early genetic changes, which does not demonstrate any histological alterations, thus explaining the concept of field cancerization due to which the mRNA levels of STs and sialidase are higher. In contrast to our results, increased mRNA levels of various STs and sialidase transcripts have been reported in cervical cancer, colorectal cancer, renal carcinoma, gastric cancer, and pancreatic carcinoma …”

Section: Discussioncontrasting

confidence: 99%

“Aberrant sialylation plays a significant role in oral squamous cell carcinoma progression”

Mehta

Patel

Pandya

et al. 2020

J Oral Pathology Medicine

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Objective Aberrant glycosylation, mainly sialylation and fucosylation, is recently considered as a major hallmark of cancer. Aberrant sialylation has long been associated with various neoplastic diseases. However, role of aberrant sialylation in oral cancer is still in its infancy. The present study aimed to examine mRNA expressions of α‐2, 3, α‐2, 6 sialyltransferase (ST) families and sialidase in 160 human oral cancer tissues. Methods mRNA expression of ST3GAL1, ST3GAL2, ST3GAL3, ST3GAL4, ST3GAL6, ST6GAL1, and neuraminidase 3 (NEU3) was analyzed by RT‐qPCR in 80 paired malignant and adjacent normal tissues from oral cancer patients. Results The results indicated significant (P ≤ .05) down‐regulation of various STs (ST3GAL1, ST3GAL2, ST3GAL3, ST3GAL4, ST3GAL6, and ST6GAL1) and sialidases (NEU3) in malignant tissues as compared to adjacent normal tissues. Higher mRNA levels of ST3GAL2 and ST3GAL3 were significantly associated with advanced stage of the disease, lymph node involvement, and perineural invasion, which denote their role in progression and metastasis of oral cancer. Present study also revealed altered sialylation patterns according to anatomical site of the disease and tobacco habit. Conclusion The study demonstrated significant role of elevated mRNA levels of ST3GAL2 and ST3GAL3 in disease progression and metastasis of oral carcinoma.

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Section: Discussioncontrasting

confidence: 99%

“Aberrant sialylation plays a significant role in oral squamous cell carcinoma progression”

Mehta

Patel

Pandya

et al. 2020

J Oral Pathology Medicine

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“…Aberrant sialylations have been associated with a number of processes, including adhesion, tumor progression and metastasis (7,37,38). In addition, ST3Gal3 and ST6Gal1 play roles in cisplatin-resistance, as previously reported (30,31,39). However, the combination of cisplatin and paclitaxel serves as a standard chemotherapy regimen for patients with advanced ovarian cancer (40,41).…”

Section: Discussionsupporting

confidence: 83%

ST3Gal3 confers paclitaxel‑mediated chemoresistance in ovarian cancer cells by attenuating caspase‑8/3 signaling

et al. 2019

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The aberrant expression of sialyltransferase has a role in cell differentiation, neoplastic transformation and the progression of various types of cancer. Our previous studies have shown that high expression of β-galactoside-α2,3-sialyltransferase III (ST3Gal3) in the metastatic ovarian cancer cell line HO8910PM attenuated cisplatin-induced apoptosis. The present study demonstrated that paclitaxel-induced chemoresistance in ovarian cancer cells upregulated the expression of ST3Gal3 and reduced the activity of caspase-8/3. The results of the present study revealed that the endogenous levels of ST3Gal3 mRNA and protein were significantly higher in HO8910PM cells compared with SKOV3 cells. A higher expression of ST3Gal3 was correlated with an increased resistance to paclitaxel, while the downregulation of ST3Gal3 resulted in paclitaxel-induced apoptosis. Paclitaxel upregulated ST3Gal3 expression at the mRNA and protein levels in HO8910PM cells, but not in SKOV3 cells. Silencing of ST3Gal3 by small interfering RNA reversed these effects and increased the protein levels of caspase-8/3, which may contribute to paclitaxel-induced apoptosis. The results of the present study suggested that ST3Gal3 was a target for paclitaxel-related resistance during ovarian cancer chemotherapy.

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“…62 ST6GAL1, however, is often found overexpressed in resistant cell lines. [63][64][65] Some groups have hypothesized that increased sialylation might affect TNF activation or affect the MAP-kinase/caspase pathway increasing cell death resistance. 66,67 The results point to a switch from an epithelial to a mesenchymal phenotype, which is corroborated by the increased cell mobility demonstrated in Figure 10.…”

Section: Discussionmentioning

confidence: 99%

Resistance to paclitaxel induces glycophenotype changes and mesenchymal-to-epithelial transition activation in the human prostate cancer cell line PC-3

et al. 2020

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The development of the multidrug resistance phenotype is one of the major challenges faced in the treatment of cancer. The multidrug resistance phenotype is characterized by cross-resistance to drugs with different chemical structures and mechanisms of action. In this work, we hypothesized that the acquisition of resistance in cancer is accompanied by activation of the epithelial-to-mesenchymal transition process, where the tumor cell acquires a more mobile and invasive phenotype; a fundamental step in tumor progression and in promoting the invasion of other organs and tissues. In addition, it is known that atypical glycosylations are characteristic of tumor cells, being used as biomarkers. We believe that the acquisition of the multidrug resistance phenotype and the activation of epithelial-to-mesenchymal transition provoke alterations in the cell glycophenotype, which can be used as glycomarkers for chemoresistance and epithelial-to-mesenchymal transition processes. Herein, we induced the multidrug resistance phenotype in the PC-3 human prostate adenocarcinoma line through the continuous treatment with the drug paclitaxel. Our results showed that the induced cell multidrug resistance phenotype (1) acquired a mixed profile between epithelial and mesenchymal phenotypes and (2) modified the glycophenotype, showing an increase in the level of sialylation and in the number of branched glycans. Both mechanisms are described as indicators of poor prognosis.

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Knockdown of ST6Gal-I increases cisplatin sensitivity in cervical cancer cells

Cited by 26 publications

References 46 publications

“Aberrant sialylation plays a significant role in oral squamous cell carcinoma progression”

“Aberrant sialylation plays a significant role in oral squamous cell carcinoma progression”

ST3Gal3 confers paclitaxel‑mediated chemoresistance in ovarian cancer cells by attenuating caspase‑8/3 signaling

Resistance to paclitaxel induces glycophenotype changes and mesenchymal-to-epithelial transition activation in the human prostate cancer cell line PC-3

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