Alpha-fetoprotein stimulated the expression of some oncogenes in human hepatocellular carcinoma Bel 7402 cells

Li, Mengsen; Li, Pingfeng; Chen, Qian; Du, Gangjun; Li, Gang

doi:10.3748/wjg.v10.i6.819

Cited by 51 publications

(37 citation statements)

References 28 publications

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“…Research shows that the inactivated ERK1/2 is located in the cytoplasm and activated ERK1/2 is translocated to the nucleus (16). It will then enhance the expression of certain oncogenes, including proliferation factors (17). Furthermore, the activation of JNK and p38 was hypothesized to inhibit cell apoptosis through the inactivation of caspase-3 (18,19).…”

Section: Discussionmentioning

confidence: 99%

Paclitaxel induces apoptosis and reduces proliferation by targeting epidermal growth factor receptor signaling pathway in oral cavity squamous cell carcinoma

Zhang

Wang

et al. 2015

Oncology Letters

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Abstract. Oral cavity cancer is common worldwide. Furthermore, the epidermal growth factor receptor (EGFR) signaling pathway is considered to be constitutively activated in oral cancers. Paclitaxel is widely accepted as an antitumor drug as it effectively inhibits the cell cycle. This study predominantly explores the possible molecule mechanism of paclitaxel on oral cancer treatment. Cell viability was first detected using an MTT assay. Cell apoptosis was examined by Hoechst staining and flow cytometry using an annexin-V and propidium iodide kit. Specific EGFR signaling pathways were further explored through western blot analysis. Abnormal protein expression levels were determined via immunofluoresence. Additionally, the protein levels of matrix metalloproteinase (MMP)-2 and 9 were determined using ELISA. Paclitaxel significantly inhibited oral cancer cell viability in a time-and dose-dependent manner. Paclitaxel also enhanced oral cancer cell apoptosis via increased Bim and Bid protein expression. Furthermore, paclitaxel was observed to inhibit oral cancer cell proliferation through increased MMP-2 and MMP-9 protein levels. Paclitaxel inhibited the growth of the oral cancer cell line, tea8113 malignant proliferation and enhanced tea8113 cell apoptosis through inhibiting the EGFR signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Paclitaxel induces apoptosis and reduces proliferation by targeting epidermal growth factor receptor signaling pathway in oral cavity squamous cell carcinoma

Zhang

Wang

et al. 2015

Oncology Letters

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“…Wang and Xie et al [31] showed that AFP enhances the proliferation of human HCC cells, and they suggested that this effect was mediated by an AFP/receptor autocrine pathway. In addition, AFP stimulates the expression of some oncogenes in human HCC cells and has immunosuppressive activity [32,33]. These results suggest that not only hepatic inflammation accompanied by elevation of serum AFP level, but AFP itself, is associated with hepatocarcinogenesis.…”

Section: Discussionmentioning

confidence: 92%

Serum Alpha-Fetoprotein Levels During and After Interferon Therapy and the Development of Hepatocellular Carcinoma in Patients with Chronic Hepatitis C

et al. 2008

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The association between serum alpha-fetoprotein (AFP) levels during and after interferon (IFN) therapy and the development of hepatocellular carcinoma (HCC) was evaluated in patients with chronic hepatitis C (CHC). A total of 263 patients treated by IFN with or without ribavirin were enrolled in the study. Serum AFP levels during and after IFN therapy were investigated retrospectively, and statistical analysis was performed to identify the factors associated with HCC development. During IFN therapy, serum AFP levels significantly decreased, regardless of virologic response to treatment. Increased serum AFP levels (>or=10 ng/ml) at the end of IFN therapy (EOT) was a close-to-significant variable affecting the development of HCC (P = 0.057), and a significantly higher cumulative incidence of HCC was seen in patients with increased serum AFP levels at EOT (P = 0.021). Serum AFP level at EOT is a possible predictor of HCC in CHC patients after IFN therapy.

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“…To this end, reports have shown that AFP can induce the expression of certain oncogenes in cell cultures of HCC. For example, it has been demonstrated that AFP could stimulate the mRNA expression of c-fos, c-jun, N-ras and mutated forms of p53 and p21 (ras) after 6-12 h incubation in HHC cell cultures [24]. Hence, AFP was found capable of promoting the expression of certain oncogenes to enhance cell growth and proliferation of human liver cancer cells.…”

Section: Activation Of Nuclear Proto-oncogenesmentioning

confidence: 99%

Alpha-Fetoprotein (AFP) and Inflammation: Is AFP an Acute and/or Chronic Phase Reactant?

2015

J Hematol Thrombo Dis

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Even though alpha-fetoprotein has long been implicated with inflammation during pregnancy and adult liver dysfunction, the literature lacks a review of such a relationship. Clarification of the role of alpha-fetoprotein in the inflammatory response is explored in the present report regarding AFP's participation as a positive and/or negative phase inflammatory reactant. Inflammation follows a complex succession of vascular changes involving alternations in blood and lymphatic vessels both at local intracellular sites and at the organ (liver) level. The inflammatory response may result in either an acute phase or develop into a chronic phase following injury or insult from foreign bodies, microbes, toxins, carcinogens, or autoimmune self-antigens. The site of inflammation attracts pleiomorphic cell infiltrates which secrete various chemical mediators such as cytokines, chemokines, interferons, histamines, and a host of others. It is herein demonstrated that alpha-fetoprotein can serve both as an acute and a chronic phase reactant depending on its stage of ontogeny. It was found that alpha-fetoprotein functions as a positive acute phase reactant in the embryo, fetus, and placenta during pregnancy. In contrast, alpha-fetoprotein proceeds to function as a negative acute phase protein in the postnatal and adult periods of life, especially following liver dysfunction and toxic insult. In chronic viral-induced inflammation of the liver, especially viral hepatitis, alpha-fetoprotein appears to serve as a positive phase inflammatory reactant.

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Alpha-fetoprotein stimulated the expression of some oncogenes in human hepatocellular carcinoma Bel 7402 cells

Cited by 51 publications

References 28 publications

Paclitaxel induces apoptosis and reduces proliferation by targeting epidermal growth factor receptor signaling pathway in oral cavity squamous cell carcinoma

Paclitaxel induces apoptosis and reduces proliferation by targeting epidermal growth factor receptor signaling pathway in oral cavity squamous cell carcinoma

Serum Alpha-Fetoprotein Levels During and After Interferon Therapy and the Development of Hepatocellular Carcinoma in Patients with Chronic Hepatitis C

Alpha-Fetoprotein (AFP) and Inflammation: Is AFP an Acute and/or Chronic Phase Reactant?

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