HPV 诱导的癌变和癌症恶病质中长链非编码 RNA 的表达：在 K14-HPV16 小鼠中的研究。

Expression of LncRNAs in HPV-induced Carcinogenesis and Cancer Cachexia: A Study in K14-HPV16 Mice.

机构信息

Molecular Oncology and Viral Pathology Group, Research Center of IPO Porto (CI-IPOP)/RISE@CI-IPOP (Health Research Network), Portuguese Oncology Institute of Porto (IPO Porto)/Porto Comprehensive Cancer Center (Porto.CCC), Porto, Portugal.

Faculty of Medicine of the University of Porto (FMUP), Porto, Portugal.

出版信息

Anticancer Res. 2022 May;42(5):2443-2460. doi: 10.21873/anticanres.15723.

DOI:10.21873/anticanres.15723

PMID:35489755

Abstract

AIM

To evaluate the expression of lincRNA-p21, H19, EMX2OS, SNHG12 and MALAT1 in a mouse model of human papillomavirus 16 (HPV16)-induced carcinogenesis and cachexia.

MATERIALS AND METHODS

Chest skin, ear, tongue, penis and gastrocnemius muscle samples from wild-type mice (HPV-) and K14-HPV16 male mice (HPV+) were collected to evaluate the expression of the selected lncRNAs using real-time PCR (qPCR).

RESULTS

In chest skin and ear, H19, SNHG12, EMX2OS and lincRNA-p21 were down-regulated in HPV+ versus HPV- mice. In tongue and penile tissues, there was only down-regulation of lincRNA-p21 in HPV+ mice. Additionally, in penile tissue, lincRNA-p21 expression decreased in HPV-induced lesions comparing with normal tissues. In gastrocnemius muscle, MALAT1 was up-regulated and lincRNA-p21 was down-regulated in HPV+ versus HPV-mice.

CONCLUSION

H19, SNHG12, EMX2OS and lincRNA-p21 may be involved in HPV-induced carcinogenesis. In addition, MALAT1 and lincRNA-p21 may play a role in muscle wasting and contribute to cancer cachexia.

摘要

目的

评估长链非编码 RNA（lncRNA）-p21、H19、EMX2OS、SNHG12 和 MALAT1 在人乳头瘤病毒 16（HPV16）诱导的致癌作用和恶病质的小鼠模型中的表达。

材料和方法

采集野生型小鼠（HPV-）和 K14-HPV16 雄性小鼠（HPV+）的胸皮、耳、舌、阴茎和腓肠肌样本，采用实时 PCR（qPCR）评估所选 lncRNA 的表达。

结果

在胸皮和耳部，HPV+小鼠中 H19、SNHG12、EMX2OS 和 lincRNA-p21 的表达下调。在舌和阴茎组织中，仅在 HPV+小鼠中下调了 lincRNA-p21。此外，在阴茎组织中，与正常组织相比，HPV 诱导的病变中 lincRNA-p21 的表达降低。在腓肠肌中，HPV+小鼠中 MALAT1 上调，lincRNA-p21 下调。