Aldolase B inhibits metastasis through Ten–Eleven Translocation 1 and serves as a prognostic biomarker in hepatocellular carcinoma

Tao, Qi-Fei; Yuan, Shengxian; Yang, Fusheng; Yang, Siwei; Yang, Yuan; Yuan, Ji‐hang; Wang, Zhenguang; Xu, Qingguo; Lin, Kongying; Cai, Jie; Yu, Jian; Huang, Weijian; Teng, Xiaolei; Zhou, Chuanchuan; Wang, Fang; Sun, Shuhan; Zhou, Weiping

doi:10.1186/s12943-015-0437-7

Cited by 69 publications

(78 citation statements)

References 45 publications

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“…Furthermore, Aldolase B under-expression in HCC was significantly associated with adverse clinico-pathological characteristics and worse recurrence-free survival and overall survival in both univariate and multivariate analyses (all P < .05) 15. By using HCC cell lines for in vitro and in vivo study in the same article, over-expression of Aldolase B was also negatively correlated with cell migration in vitro and occurrence of lung metastasis and intrahepatic metastasis, as well as the numbers of circulating tumor cells in vivo 15. On the contrary, up-regulation and over-expression of ALDOB gene and Aldolase B protein were detected in human tissue of pseuomyxoma peritonei (PMP) 18.…”

Section: Discussionmentioning

confidence: 92%

“…Nevertheless, down-regulation of ALDOB gene or Aldolase B protein were frequently observed in HCC tissues 13, 14, 16, 33-35. Furthermore, Aldolase B under-expression in HCC was significantly associated with adverse clinico-pathological characteristics and worse recurrence-free survival and overall survival in both univariate and multivariate analyses (all P < .05) 15. By using HCC cell lines for in vitro and in vivo study in the same article, over-expression of Aldolase B was also negatively correlated with cell migration in vitro and occurrence of lung metastasis and intrahepatic metastasis, as well as the numbers of circulating tumor cells in vivo 15.…”

Section: Discussionmentioning

confidence: 93%

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High Expression of Aldolase B Confers a Poor Prognosis for Rectal Cancer Patients Receiving Neoadjuvant Chemoradiotherapy

Tian¹,

Hsieh²,

Lin³

et al. 2017

J. Cancer

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Background: Colorectal cancer is the third most common cancer in both sex worldwide and it is also the fourth most common cause of cancer mortality. For rectal cancer, neoadjuvant concurrent chemoradiotherapy (CCRT) followed by radical proctectomy is gold standard treatment for patients with stage II/III rectal cancer. By data mining a documented database of rectal cancer transcriptome (GSE35452) from Gene Expression Omnibus, National Center of Biotechnology Information, we recognized that ALDOB was the most significantly up-regulated transcript among those related to glycolysis (GO: 0006096). Hence, we analyzed the clinicopathological correlation and prognostic effect of ALDOB protein (Aldolase B), which encoded by ALDOB gene.Methods: ALDOB immunostain was performed in 172 rectal adenocarcinomas treated with preoperative chemoradiotherapy followed by radical surgery, which were divided into high- and low-expression groups. Furthermore, statistical analyses were examined to correlate the relationship between ALDOB immunoreactivity and important clinical and pathological characteristics, as well as three survival indices: disease-specific survival (DSS), local recurrence-free survival (LRFS) and metastasis-free survival (MeFS).Results: ALDOB (Aldolase B) over-expression was significantly associated with pre-CCRT and post-CCRT tumor advancement, lymphovascular invasion, perineural invasion and poor response to CCRT (all P ≤ .023). In addition, ALDOB high expression was linked to adverse DSS, LRFS and MeFS in univariate analysis (P ≤ .0075) and also served as an independent prognosticator indicating dismal DSS and MeFS in multivariate analysis (hazard ratio (HR) = 3.462, 95% confidence interval (CI): 1.263-9.495; HR = 2.846, 95% CI: 1.190-6.808, respectively).Conclusion: ALDOB (Aldolase B) may play an imperative role in rectal cancer progression and responsiveness to neoadjuvant CCRT, and serve as a novel prognostic biomarker. Additional researches to clarify the molecular and biochemical pathways are essential for developing promising ALDOB-targeted therapies for patients with rectal cancers.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 93%

High Expression of Aldolase B Confers a Poor Prognosis for Rectal Cancer Patients Receiving Neoadjuvant Chemoradiotherapy

Tian¹,

Hsieh²,

Lin³

et al. 2017

J. Cancer

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“…Although the role of aldolase in metabolism is well established, there is growing evidence for many alternative functions of this enzyme. In particular, aldolase interacts with various proteins unrelated to glycolytic enzymes, including F-actin [23], ARNO [24], tubulin [25] and is crucial for proliferation [26] and invasion [27] of cancer cells through a non-glycolytic pathway. In the present study, ALDOB was highly expressed in CRC and its expression was correlated with tumor stage.…”

Section: Discussionmentioning

confidence: 99%

Aldolase B Overexpression is Associated with Poor Prognosis and Promotes Tumor Progression by Epithelial-Mesenchymal Transition in Colorectal Adenocarcinoma

Li¹,

Li²,

et al. 2017

Cell Physiol Biochem

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Background: Glycolysis is considered to be the root of cancer development and progression, which involved a multi-step enzymatic reaction. Our study aimed at figuring out which glycolysis enzyme participates in the development of colorectal cancer and its possible mechanisms. Methods: We firstly screened out Aldolase B (ALDOB) by performing qRT-PCR arrays of glycolysis-related genes in five paired liver metastasis and primary colorectal tissues, and further detected ALDOB protein with immunohistochemistry in tissue microarray (TMA) consisting of 229 samples from stage I-III colorectal cancer patients. CRISPR-Cas9 method was adopted to create knock out colon cancer cell lines (LoVo and SW480) of ALDOB. The effect of ALDOB on cell proliferation and metastasis was examined in vitro using colony formation assay as well as transwell migration and invasion assay, respectively. Results: In TMA, there was 64.6% of samples demonstrated strong intensity of ALDOB. High ALDOB expression were associated with poor overall survival and disease-free survival in both univariate and multivariate regression analyses (P<0.05). In vitro functional studies of CCK-8 demonstrated that silencing ALDOB expression significantly (P<0.05) inhibited proliferation, migration and invasion of colon cancer cells. Mechanically, silencing ALDOB activated epithelial markers and repressed mesenchymal markers, indicating inactivation of ALDOB may lead to inhibition of epithelial-mesenchymal transition (EMT). Conclusion: Upregulation of ALDOB promotes colorectal cancer metastasis by facilitating EMT and acts as a potential prognostic factor and therapeutic target in colorectal cancer.Q. Li and Y. Li contributed equally to this work.

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“…The tissue microarrays and IHC were performed as previously described . After heating, the sections were incubated with primary antibody for 30 min and then with the secondary antibody for an hour at room temperature.…”

Section: Methodsmentioning

confidence: 99%

Overactivated neddylation pathway in human hepatocellular carcinoma

Huang

et al. 2018

Cancer Medicine

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Dysregulation of the neddylation pathway is related to various cancers. However, the specific role of the neddylation pathway in human hepatocellular carcinoma (HCC) remains largely unclear. In this study, the neddylation pathway in HCC and adjacent noncancerous liver (ANL) tissues was evaluated by immunohistochemistry (IHC), Western blotting, and qRT‐PCR (quantitative real‐time polymerase chain reaction). The results showed that the entire neddylation pathway, including NEDD8 (the IHC staining of NEDD8 represents the global‐protein neddylation), E1 NEDD8‐activating enzymes (NAE1 and UBA3), E2 NEDD8‐conjugating enzymes (UBE2F and UBE2M), E3 NEDD8‐ligases (MDM2, RBX1 and RNF7), and deneddylation enzymes (COPS5, UCHL1 and USP21), was overactivated in HCC. Furthermore, the upregulation of NEDD8 in HCC was correlated with aggressive characteristics and was an independent risk factor for overall survival (OS) and recurrence‐free survival (RFS) in patients with HCC after hepatectomy. The upregulation of NAE1, UBE2M, and UCHL1 in HCC was associated with aggressive characteristics and poor OS and RFS in patients with HCC after hepatectomy. In conclusion, our research reveals that the entire neddylation pathway is overactivated in HCC and associated with clinical characteristics and prognosis of patients with HCC.

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Aldolase B inhibits metastasis through Ten–Eleven Translocation 1 and serves as a prognostic biomarker in hepatocellular carcinoma

Cited by 69 publications

References 45 publications

High Expression of Aldolase B Confers a Poor Prognosis for Rectal Cancer Patients Receiving Neoadjuvant Chemoradiotherapy

High Expression of Aldolase B Confers a Poor Prognosis for Rectal Cancer Patients Receiving Neoadjuvant Chemoradiotherapy

Aldolase B Overexpression is Associated with Poor Prognosis and Promotes Tumor Progression by Epithelial-Mesenchymal Transition in Colorectal Adenocarcinoma

Overactivated neddylation pathway in human hepatocellular carcinoma

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