RETRACTED ARTICLE: α2,6-Sialylation mediates hepatocellular carcinoma growth in vitro and in vivo by targeting the Wnt/β-catenin pathway

Zhao, Yujie; Wei, Anwen; Zhang, H; Chen, X; Wang, L; Yu, Xiao; Yuan, Qingmin; Zhang, J; Wang, S

doi:10.1038/oncsis.2017.40

Cited by 17 publications

(17 citation statements)

References 38 publications

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“…Moreover, its expression has been associated with changes in adhesion, metastasis and poor prognosis . In our previous work, we demonstrated that ST6Gal‐I may act as a tumor promoter in hepatocarcinoma and prostate cancer cells . In the present study, we demonstrated that silencing of ST6Gal‐I resulted in reduced cell proliferation, clonogenic, migration and invasion ability of A549 and H1299 NSCLC cells in vitro , which could be rescued by the reintroduction of ST6Gal‐I and Notch1.…”

Section: Discussionsupporting

confidence: 59%

“…Effects of ST6Gal‐I on cancer progression is quite controversial, being either inhibitive or facilitative. ST6Gal‐I overexpression has been reported in several types of cancer, including liver, prostate, ovarian and colorectal carcinomas . Our previous study found that ST6Gal‐I improved hepatocarcinoma cells (HCC) proliferation, migration and invasion, and modulated docetaxel sensitivity in HCC via the p38 MAPK/caspase pathway .…”

mentioning

confidence: 99%

“…[19][20][21][22] Our previous study found that ST6Gal-I improved hepatocarcinoma cells (HCC) proliferation, migration and invasion, and modulated docetaxel sensitivity in HCC via the p38 MAPK/caspase pathway. 19,23 On the other hand, ST6Gal-I overexpression inhibited the cell migration and increased the cell death induced by chemotherapeutic drugs in glioma cells. 24,25 However, the function of ST6Gal-I in NSCLC and the molecular mechanisms involved in lung cancer progression remain unclear.…”

mentioning

confidence: 99%

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Modification of α2,6‐sialylation mediates the invasiveness and tumorigenicity of non‐small cell lung cancer cells in vitro and in vivo via Notch1/Hes1/MMPs pathway

Yuan

Chen

Han

et al. 2018

Intl Journal of Cancer

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The alterations of sialylation on cell surface N-glycans due to overexpression of different sialyltransferases play a vital role in tumorigenesis and tumor progression. The β-galactoside α2-6-sialyltransferase 1 (ST6Gal-I) has been reported to be highly expressed in several cancers, including breast cancer, hepatocellular cancer and colon carcinoma. However, the roles and underlying mechanisms of ST6Gal-I in non-small cell lung cancer (NSCLC) still need to be elucidated. In this study, we determined that mRNA levels of ST3GAL1, ST6GALNAC3 and ST8SIA6 were remarkably reduced in lung cancer tissues and cells, whereas ST6GAL1 level significantly increased. The mRNA, protein and glycan levels of ST6Gal-I were higher in lung cancer tissues and cells. Moreover, down-regulation of ST6Gal-I decreased protein levels of Jagged1, DLL-1, Notch1, Hes1, Hey1, matrix-metalloproteinases (MMPs) and VEGF, and suppressed proliferation, migration and invasion capabilities of A549 and H1299 cells in vitro. In vivo, ST6Gal-I silencing suppressed tumorigenicity of NSCLC cells in athymic nude mice via the Notch1/Hes1/MMPs pathway. In addition, overexpression of Notch1 rescued the reduced growth and metastasis of A549 and H1299 cells resulted by ST6Gal-I silencing. Modification of α2,6-sialylation positively associates with lung cancer progression, thereby indicating that ST6Gal-I may mediate the invasiveness and tumorigenicity of NSCLC cells via the Notch1/Hes1/MMPs pathway both in vitro and in vivo. Thus, our results provide a novel therapeutic approach for blocking metastasis in lung cancer patients.

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Section: Discussionsupporting

confidence: 59%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Modification of α2,6‐sialylation mediates the invasiveness and tumorigenicity of non‐small cell lung cancer cells in vitro and in vivo via Notch1/Hes1/MMPs pathway

Yuan

Chen

Han

et al. 2018

Intl Journal of Cancer

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“…Furthermore, a former study has demonstrated that SOX9 can regulate Wnt/β‐catenin pathway to promote stemness in HCC (Leung et al ., ). The Wnt/β‐catenin pathway has been largely reported as crucial signaling in the regulation of progression and metastases in HCC (Chao et al ., ; Hu et al ., ; Zhao et al ., ). Therefore, we wondered whether SOX9 and SOX9‐AS1 could regulate the Wnt/β‐catenin pathway in HCC.…”

Section: Resultsmentioning

confidence: 97%

“…Additionally, several studies have reported that SOX9 could regulate the Wnt/β‐catenin pathway in human cancers (Cui et al ., ; Guo et al ., ; Santos et al ., ), including HCC (Leung et al ., ). The Wnt/β‐catenin pathway has been recognized as a key pathway implicated in HCC progression and metastasis (Chao et al ., ; Hu et al ., ; Zhao et al ., ). Herein, we showed that silencing SOX9 or SOX9‐AS1 could attenuate the Wnt/β‐catenin pathway, thereby inhibiting EMT.…”

Section: Discussionmentioning

confidence: 97%

A SOX9‐AS1/miR‐5590‐3p/SOX9 positive feedback loop drives tumor growth and metastasis in hepatocellular carcinoma through the Wnt/β‐catenin pathway

Zhang

Hou

et al. 2019

Molecular Oncology

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Hepatocellular carcinoma (HCC) is a prevalent solid tumor with a high global death rate. SRY box 9 (SOX9) has been reported as an oncogene in HCC by several studies, but the underlying mechanism remains largely unexplored. Here, we confirmed upregulation of SOX9 in HCC tissues and cell lines and validated that SOX9 facilitates proliferation, migration and invasion in HCC. We subsequently identified that the long non‐coding RNA (lncRNA) SOX9 antisense RNA 1 (SOX9‐AS1) is a neighbor gene to SOX9; SOX9‐AS1 is also upregulated in HCC, and its expression is positively correlated with that of SOX9. In addition, SOX9‐AS1 appears to have prognostic significance in HCC patients. We showed that SOX9‐AS1 aggravates HCC progression and metastasis in vitro and in vivo. We demonstrated that SOX9‐AS1 sponges miR‐5590‐3p to elevate SOX9 expression, and that SOX9 in turn transcriptionally activates SOX9‐AS1. Moreover, we verified that SOX9‐AS1 regulates SOX9 and its known downstream Wnt/β‐catenin pathway so as to facilitate epithelial‐to‐mesenchymal transition. The results of our rescue assays suggest that SOX9‐AS1 regulates HCC progression through SOX9 and the Wnt/β‐catenin pathway. In conclusion, our study demonstrates that a SOX9‐AS1/miR‐5590‐3p/SOX9 positive feedback loop drives tumor growth and metastasis in HCC through the Wnt/β‐catenin pathway, suggesting SOX9‐AS1 as a novel potential prognostic and treatment target for HCC.

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Serum sialylation changes in cancer

2018

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Cancer is a major cause of death in both developing and developed countries. Early detection and efficient therapy can greatly enhance survival. Aberrant glycosylation has been recognized to be one of the hallmarks of cancer as glycans participate in many cancer-associated events. Cancer-associated glycosylation changes often involve sialic acids which play important roles in cell-cell interaction, recognition and immunological response. This review aims at giving a comprehensive overview of the literature on changes of sialylation in serum of cancer patients. Furthermore, the methods available to measure serum and plasma sialic acids as well as possible underlying biochemical mechanisms involved in the serum sialylation changes are surveyed. In general, total serum sialylation levels appear to be increased with various malignancies and show a potential for clinical applications, especially for disease monitoring and prognosis. In addition to overall sialic acid levels and the amount of sialic acid per total protein, glycoprofiling of specific cancer-associated glycoproteins, acute phase proteins and immunoglobulins in serum as well as the measurements of sialylation-related enzymes such as sialidases and sialyltransferases have been reported for early detection of cancer, assessing cancer progression and improving prognosis of cancer patients. Moreover, sialic-acid containing glycan antigens such as CA19–9, sialyl Lewis X and sialyl Tn on serum proteins have also displayed their value in cancer diagnosis and management whereby increased levels of these factors positively correlated with metastasis or poor prognosis.

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RETRACTED ARTICLE: α2,6-Sialylation mediates hepatocellular carcinoma growth in vitro and in vivo by targeting the Wnt/β-catenin pathway

Cited by 17 publications

References 38 publications

Modification of α2,6‐sialylation mediates the invasiveness and tumorigenicity of non‐small cell lung cancer cells in vitro and in vivo via Notch1/Hes1/MMPs pathway

Modification of α2,6‐sialylation mediates the invasiveness and tumorigenicity of non‐small cell lung cancer cells in vitro and in vivo via Notch1/Hes1/MMPs pathway

A SOX9‐AS1/miR‐5590‐3p/SOX9 positive feedback loop drives tumor growth and metastasis in hepatocellular carcinoma through the Wnt/β‐catenin pathway

Serum sialylation changes in cancer

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