Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells

Zhu, Mingyue; Guo, Junli; Xia, Hua; Li, Wei; Lü, Yan; Xu, Dong; Chen, Yi; Xie, Xieju; Fu, Shigan; Li, Mengsen

doi:10.18632/oncoscience.115

Cited by 41 publications

(35 citation statements)

References 37 publications

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“…Previous study have found that suppressed expression of AFP maybe inhibit the transduction of PI3K/AKT signal pathway in HCC cells [42], we found that AFP harbored the ability to activate the PI3K/AKT signalling pathway to promote CXCR4, Src, Ras, MMP2/9, and K19 expression and to stimulate the proliferation and metastasis of HCC cells [32, 33–36, 43]. AFP also promoted malignant behaviors and antagonized the apoptosis induced by paclitaxel in hepatoma cells [44, 45].…”

Section: Discussionmentioning

confidence: 75%

Alpha fetoprotein antagonises benzyl isothiocyanate inhibition of the malignant behaviors of hepatocellular carcinoma cells

Zhu

Guo

et al. 2016

Oncotarget

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Benzyl isothiocyanate (BITC) is a dietary isothiocyanate derived from cruciferous vegetables. Recent studies showed that BITC inhibited the growth of many cancer cells, including hepatocellular carcinoma (HCC) cells. Alpha-fetoprotein (AFP) is a important molecule for promoting progression of HCC, in the present investigation, we explore the influence of AFP on the role of BITC in the malignant behaviours of HCC cells, and the potential underlying mechanisms. We found thatBITC inhibited viability, migration, invasion and induced apoptosis of human liver cancer cell lines, Bel 7402(AFP producer) and HLE(non-AFP producer) cells in vitro. The role of BITC involve in promoting actived-caspase-3 and PARP-1 expression, and enhancing caspase-3 activity but decreasing MMP-2/9, survivin and CXCR4 expression. AFP antagonized the effect of BITC. This study suggests that BITC induced significant reductions in the viability of HCC cell lines. BITC may activate caspase-3 signal and inhibit the expression of growth- and metastasis-related proteins; AFP is an pivotal molecule for the HCC chemo-resistance of BITC.

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Section: Discussionmentioning

confidence: 75%

Alpha fetoprotein antagonises benzyl isothiocyanate inhibition of the malignant behaviors of hepatocellular carcinoma cells

Zhu

Guo

et al. 2016

Oncotarget

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“…Univariate analysis identified that factors associated with tumor progression following a single TACE treatment included AFP, pre-TACE CD151 and post-TACE CD151. A previous study demonstrated that AFP may promote AKT phosphorylation through interaction with the phosphatase and tensin homolog protein, thereby increasing the expression of the C-X-C chemokine receptor type 4 (CXCR4) protein (also known as stromal-derived factor-1α) (31). At the same time, mechanistic target of rapamycin enters the nucleus to combine with the CXCR4 gene promoter, which promotes the growth and metastasis of HCC (28).…”

Section: Discussionmentioning

confidence: 99%

Expression of cluster of differentiation 151 prior to and following transcatheter arterial chemoembolization therapy in patients with hepatocellular carcinoma and its association with clinicopathological characteristics

Kang

Xiao

2017

Oncol Lett

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Abstract. Cluster of differentiation (CD)151, a member of tetraspanin family, is considered to be the first tetraspanin to be associated with tumor metastasis. Previous studies in vivo, in vitro and in the clinic have demonstrated that CD151 is involved in tumor progression at different levels through interaction with integrins, growth factor receptors and matrix metalloproteinases. Transcatheter arterial chemoembolization (TACE) is widely recommended for the treatment of patients with advanced hepatocellular carcinoma (HCC) worldwide. It has been hypothesized that TACE may create a hypoxic-ischemic environment that increases the expression of tumor progression-associated factors, promotes the angiogenesis of HCC, and initiates the recurrence and metastasis of HCC. Whether TACE promotes HCC progression remains controversial and numerous studies have focused on the influence of TACE on a number of tumor progression-associated factors. In the present study, the expression of serum CD151 in patients with HCC prior to and following TACE and its association with clinicopathological characteristics was investigated. It was revealed that the expression level of CD151 at 5-7 days post-TACE was significantly increased compared with pre-TACE levels. Risk factors and protective factors associated with tumor progression following a single TACE procedure and 18 months of follow-up were also identified. Furthermore, the present study revealed that a pre-TACE CD151 level of >0.3247 ng/ml and a 5-7 days post-TACE CD151 level of >0.3146 ng/ml revealed moderate sensitivity and specificity for predicting HCC progression following a single TACE procedure. The present study highlights CD151 as a useful marker in predicting the response to treatment and monitoring the disease course following TACE.

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“…In vitro studies further showed that recombinant CXCL12 (SDF-1) treatment expanded the population of OV6-positive HCC-initiating cells and a specific inhibition with AMD3100 or CXCR4 targeting siRNAs blocked these effects [50]. Alpha-fetoprotein (AFP), a tumor-associated fetal protein which has been described as a useful marker for HCC detection and monitoring [79], has been recently also identified to promote the migration of HCC cells through activation of the PI3K/ AKT signal pathway resulting in the expression of CXCR4 [80]. Finally, using a 3D HCC invasion culture model and quantitative proteomics techniques alongside liquid chromatography-tandem mass spectrometry (LC-MS/MS), Chen et al recently identified eight proteins involved in early invasion of HCCs including MMP2, MMP7, MMP9, CD44, SPP1, CXCR4, CXCL12, and CDH1, which showed dynamic alterations during the early invasion process of HCC [81].…”

Section: Cxcl12-cxcr4 Axismentioning

confidence: 99%

Role of chemokine pathways in hepatobiliary cancer

Ehling

Tacke

2016

Cancer Letters

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Alpha-fetoprotein activates AKT/mTOR signaling to promote CXCR4 expression and migration of hepatoma cells

Cited by 41 publications

References 37 publications

Alpha fetoprotein antagonises benzyl isothiocyanate inhibition of the malignant behaviors of hepatocellular carcinoma cells

Alpha fetoprotein antagonises benzyl isothiocyanate inhibition of the malignant behaviors of hepatocellular carcinoma cells

Expression of cluster of differentiation 151 prior to and following transcatheter arterial chemoembolization therapy in patients with hepatocellular carcinoma and its association with clinicopathological characteristics

Role of chemokine pathways in hepatobiliary cancer

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