title: Effect of Hath1 on the proliferation and apoptosis of cutaneous squamous cell carcinoma in vitro.
abstract: Increasing evidence has demonstrated that the tumor suppressor gene Hath1 is implicated in the development and progression of tumors and is verified to be downregulated in several types of tumor. However, the roles and precise molecular mechanisms of Hath1 in cutaneous squamous cell carcinoma (SCC) remain to be elucidated. In the present study, two approaches were used to investigate the tumor‑suppressing effect of Hath1 in cutaneous SCC. Firstly, the effect of inhibiting Hath1 expression with short hairpin RNA (shRNA) on tumor growth and apoptosis was investigated. KUMA5 cells were stably transfected with a plasmid expressing Hath1 shRNA (pGenesil‑1‑Hath1). Secondly, the anti‑tumor effect of Hath1 was investigated in KUMA5 cells following transfection with pcDNA3.1‑Hath1. The mRNA and protein expression of Hath1 was detected by reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively. Cell proliferation in vitro was assessed using an MTT assay. Flow cytometry was used to detect cell apoptosis. The results demonstrated that compared with the control groups, the expression of Hath1 was significantly reduced in the KUMA5/pGenesil‑1‑Hath1 cells and markedly increased in the KUMA5/pcDNA3.1‑Hath1 cells. Cell proliferation was markedly increased in the KUMA5/pGenesil‑1‑Hath1 cells in a time‑dependent manner; however, it was markedly inhibited in the KUMA5/pcDNA3.1‑Hath1 cells. Flow cytometry revealed that apoptosis decreased in KUMA5/pGenesil‑1‑Hath1 cells and increased in KUMA5/pcDNA3.1‑Hath1 cells. Downregulation of Hath1 expression promoted the proliferation and reduced the apoptosis of KUMA5 cells. By contrast, overexpression of Hath1 inhibited proliferation and induced the apoptosis of KUMA5 cells. These findings provide possible new strategies and therapeutic targets for the treatment and diagnosis of cutaneous SCC.
authors.affiliation: Department of Dermatology, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
authors.forename: Zuolin
authors.initials: Z
authors.lastname: Ying
authors.affiliation: Department of Dermatology, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
authors.forename: Xiaojie
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Dermatology, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
authors.forename: Hong
authors.initials: H
authors.lastname: Dang
authors.affiliation: Experimental Research Center, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
authors.forename: Feng
authors.initials: F
authors.lastname: Wang
authors.affiliation: Experimental Research Center, Shanghai First People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200080, P.R. China.
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Xu
mesh_terms: D017209:Apoptosis / Q000235:genetics*; D051792:Basic Helix-Loop-Helix Proteins / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000235:genetics*; D005434:Flow Cytometry; D020868:Gene Silencing; D006801:Humans
chemical_list: D051792:Basic Helix-Loop-Helix Proteins; C500942:ATOH1 protein, human