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

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

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.

Keywords: HPV; K14-HPV16; cancer cachexia; lncRNAs; muscle wasting.

MeSH terms

  • Animals
  • Cachexia / genetics
  • Carcinogenesis / genetics
  • Female
  • Human papillomavirus 16 / genetics
  • Human papillomavirus 16 / metabolism
  • Humans
  • Male
  • Mice
  • Papillomavirus Infections* / complications
  • Papillomavirus Infections* / genetics
  • Papillomavirus Infections* / metabolism
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism

Substances

  • RNA, Long Noncoding