PMID- 34738627
OWN - NLM
STAT- MEDLINE
DCOM- 20220110
LR  - 20220110
IS  - 1791-2431 (Electronic)
IS  - 1021-335X (Print)
IS  - 1021-335X (Linking)
VI  - 47
IP  - 1
DP  - 2022 Jan
TI  - Contrasting functions of the epithelial‑stromal interaction 1 gene, in human oral 
      and lung squamous cell cancers.
LID - 5 [pii]
LID - 10.3892/or.2021.8216 [doi]
AB  - The epithelial‑stromal interaction 1 gene (EPSTI1) is known to play multiple 
      roles in the malignant progression of breast cancer and also in some aspects of 
      the immune responses to the tumor. However, the relevance of the gene in the 
      onset/progression of oral squamous cell carcinoma (OSCC) and lung squamous cell 
      carcinoma (LSCC) is not yet known. The present study was aimed at revealing the 
      roles of EPSTI1 in conferring malignant characteristics to OSCC and LSCC, and the 
      underlying mechanisms. Quantitative real‑time polymerase chain reaction (PCR) and 
      western blot analyses demonstrated significant upregulation of EPSTI1 in all four 
      OSCC cell lines (HSC2, HSC3, HSC3‑M3 and HSC4), and significant downregulation of 
      EPST11 in all three LSCC cell lines (LK‑2, EBC‑1 and H226) used in the present 
      study, as compared to the expression levels in the corresponding control cell 
      lines. Both knockdown of EPST11 in OSCC and overexpression of the gene in LSCC 
      suppressed cell proliferation, and induced cell‑cycle arrest in the G1 phase, 
      with upregulation of p21 and downregulation of CDK2 and cyclin D1. Furthermore, 
      these alterations of EPST11 gene expression in the OSCC and LSCC cell lines 
      suppressed the cell migration ability and reversed the EMT phenotype of the tumor 
      cells. Collectively, while EPSTI1 appears to have oncogenic roles in OSCC, it 
      appears to exert tumor‑suppressive roles in LSCC. PCR array analyses revealed 
      some genes whose expression levels were altered along with the modified EPSTI1 
      expression in both the OSCC and LSCC cell lines. These findings suggest that 
      EPSTI1 may be a therapeutic target for both OSCC and LSCC.
FAU - Fan, Mengmeng
AU  - Fan M
AD  - Department of Medical Oncology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Arai, Makoto
AU  - Arai M
AD  - Department of Medical Oncology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Tawada, Akinobu
AU  - Tawada A
AD  - Department of Medical Oncology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Chiba, Tetsuhiro
AU  - Chiba T
AD  - Department of Gastroenterology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Fukushima, Reo
AU  - Fukushima R
AD  - Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba 
      260‑8670, Japan.
FAU - Uzawa, Katsuhiro
AU  - Uzawa K
AD  - Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba 
      260‑8670, Japan.
FAU - Shiiba, Masashi
AU  - Shiiba M
AD  - Department of Medical Oncology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Kato, Naoya
AU  - Kato N
AD  - Department of Gastroenterology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
FAU - Tanzawa, Hideki
AU  - Tanzawa H
AD  - Department of Oral Science, Graduate School of Medicine, Chiba University, Chiba 
      260‑8670, Japan.
FAU - Takiguchi, Yuichi
AU  - Takiguchi Y
AD  - Department of Medical Oncology, Graduate School of Medicine, Chiba University, 
      Chiba 260‑8670, Japan.
LA  - eng
PT  - Journal Article
DEP - 20211105
PL  - Greece
TA  - Oncol Rep
JT  - Oncology reports
JID - 9422756
RN  - 0 (EPSTI1 protein, human)
RN  - 0 (Neoplasm Proteins)
SB  - IM
MH  - Cell Cycle/genetics
MH  - Cell Line, Tumor
MH  - Cell Movement/genetics
MH  - Cell Proliferation/genetics
MH  - Down-Regulation
MH  - Gene Expression Regulation, Neoplastic
MH  - Head and Neck Neoplasms/*genetics
MH  - Humans
MH  - Lung Neoplasms/*genetics
MH  - Neoplasm Proteins/*genetics
MH  - Squamous Cell Carcinoma of Head and Neck/*genetics
MH  - Up-Regulation
PMC - PMC8600417
OTO - NOTNLM
OT  - EPSTI1
OT  - epithelial‑mesenchymal transition
OT  - lung cancer
OT  - oral cancer
OT  - squamous cell carcinoma
COIS- The authors declare that they have no competing interests.
EDAT- 2021/11/06 06:00
MHDA- 2022/01/11 06:00
PMCR- 2021/11/02
CRDT- 2021/11/05 08:41
PHST- 2020/09/17 00:00 [received]
PHST- 2020/12/23 00:00 [accepted]
PHST- 2021/11/05 08:41 [entrez]
PHST- 2021/11/06 06:00 [pubmed]
PHST- 2022/01/11 06:00 [medline]
PHST- 2021/11/02 00:00 [pmc-release]
AID - 5 [pii]
AID - OR-0-0-08216 [pii]
AID - 10.3892/or.2021.8216 [doi]
PST - ppublish
SO  - Oncol Rep. 2022 Jan;47(1):5. doi: 10.3892/or.2021.8216. Epub 2021 Nov 5.