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KSHV co-infection regulates HPV16+ cervical cancer cells pathogenesis in vitro and in vivo.

ABSTRACT: High-risk human papillomavirus (HPV) infection is the etiological agent of cervical, oral and oropharyngeal cancers. Another oncogenic virus, Kaposi sarcoma-associated herpesvirus (KSHV) can cause several human cancers arising in those immunocompromised patients. KSHV DNA has been detected in the oral cavity and the female genital tract, although its detection rate in cervical samples is relatively low. Therefore, it remains unclear about the role of KSHV co-infection in the development of HPV-related neoplasia. We recently report that KSHV infection of HPV16+ cervical cancer cell line SiHa induces several pro-inflammatory factors production while reducing HPV16 E6 and E7 expression through the manipulation of cellular microRNA function. In the current study, we focus on determining the influence of KSHV co-infection on cervical cancer cells pathogenesis in vitro and in vivo. We found that KSHV co-infection is able to maintain SiHa and/or CaSki cells pathogenesis and tumorigenesis, although hijacking HPV oncogenic proteins expression. In mechanisms, KSHV co-infection is capable of increasing Macrophage migration inhibitory factor (MIF) and its receptor CXCR2 expression from cervical cancer cells, which may contribute to cervical cancer development. Our data indicate that KSHV co-infection may act as a potential co-factor to promote HPV-related neoplasia development.

SUBMITTER: Dai L

PROVIDER: S-EPMC5934560 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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KSHV co-infection regulates HPV16+ cervical cancer cells pathogenesis <i>in vitro</i> and <i>in vivo</i>.

Dai Lu L Qiao Jing J Del Valle Luis L Qin Zhiqiang Z

American journal of cancer research 20180401 4

High-risk human papillomavirus (HPV) infection is the etiological agent of cervical, oral and oropharyngeal cancers. Another oncogenic virus, Kaposi sarcoma-associated herpesvirus (KSHV) can cause several human cancers arising in those immunocompromised patients. KSHV DNA has been detected in the oral cavity and the female genital tract, although its detection rate in cervical samples is relatively low. Therefore, it remains unclear about the role of KSHV co-infection in the development of HPV-r ...[more]

PMID: 29736315

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Project description:BACKGROUND:Chronic alcohol use often leads to malnutrition. However, how the intestinal absorption of nutrients such as glucose may be affected during moderate ethanol use has not been investigated. Glucose is absorbed via sodium (Na)-dependent glucose co-transport (SGLT1; SLC5A1) along the brush border membrane (BBM) of intestinal absorptive villus cells. OBJECTIVE:The aim of this study was to investigate how moderate alcohol consumption affects the absorption of glucose via SGLT1. METHODS:Intestinal epithelial cells (IEC-18; rat) were exposed to 8.64 mM ethanol over 1, 3, 6, and 12 h. Rats (16-wk-old, male, Sprague-Dawley) were administered 2 g/kg ethanol over 1, 3, and 6 h. Na-dependent 3H-O-methyl-d-glucose uptake was measured to assess SGLT1 activity. Na-K-ATPase activity was measured as a function of inorganic phosphate release. Protein expression was analyzed by Western blot analysis and immunohistochemical staining. RESULTS:Ethanol significantly decreased Na-dependent glucose absorption in enterocytes in vitro (ethanol treatment: 48.4% of controls at 1 h; P < 0.01) and in vivo (ethanol treatment: 60.0% of controls at 1 h; P < 0.01). Na-K-ATPase activity was significantly inhibited in vitro (ethanol treatment: 36.9% of controls at 1 h; P < 0.01) and in vivo (ethanol treatment: 42.1% of controls at 1 h; P < 0.01). Kinetic studies showed that the mechanism of inhibition of Na-glucose co-transport was secondary to a decrease in the affinity (1/Km) of the co-transporter for glucose both in vitro and in vivo. Western blots and immunohistochemistry further demonstrated unaltered amounts of SGLT1 after ethanol treatment. CONCLUSIONS:Moderate ethanol significantly decreases glucose absorption in IEC-18 cells and in villus cells of Sprague-Dawley rats. The inhibition of SGLT1 is secondary to an altered Na gradient at the cellular level and secondary to diminished affinity of the co-transporter for glucose at the protein level in the BBM. These observations may, at least in part, explain 1 possible mechanism of the onset of malnutrition associated with alcohol consumption.

Dataset Information

KSHV co-infection regulates HPV16+ cervical cancer cells pathogenesis in vitro and in vivo.

Publications

KSHV co-infection regulates HPV16+ cervical cancer cells pathogenesis <i>in vitro</i> and <i>in vivo</i>.

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