FAM107A as a tumor suppressor in esophageal squamous carcinoma inhibits growth and metastasis.


Journal

Pathology, research and practice
ISSN: 1618-0631
Titre abrégé: Pathol Res Pract
Pays: Germany
ID NLM: 7806109

Informations de publication

Date de publication:
Dec 2023
Historique:
received: 24 10 2023
revised: 07 11 2023
accepted: 10 11 2023
medline: 29 11 2023
pubmed: 18 11 2023
entrez: 17 11 2023
Statut: ppublish

Résumé

Sequence similarity Family 107 member A (FAM107A) has been recognized as a tumor suppressor of various malignancies, which suppresses tumor proliferation and metastasis. Its specific role in esophageal squamous cell carcinoma (ESCC) remains unclear. Public datasets including Gene Expression Profiling Interactive Analysis (GEPIA) and Gene Expression Omnibus (GEO), quantitative real-time PCR (qRT-PCR), and Western blot were utilized for comparative analysis of FAM107A expression between ESCC and normal tissues. The link between FAM107A and clinicopathological features, as well as prognosis determined through χ2-test, log-rank analysis, and univariate and multivariate analyses, respectively. The impact of FAM107A on ESCC cell malignant behavior was confirmed through in vitro assays, including cell counting using the Cell Counting Kit-8 (CCK-8), clonal formation, wound healing, and transwell assays. Western blot analysis was employed to assess the effects of FAM107A on tumor epithelial-mesenchymal transition (EMT) and cell cycle-related proteins. Finally, xenograft tumors were developed to investigate the influence of FAM107A on ESCC growth in vivo. FAM107A exhibited low expression in ESCC tissues. Reduced FAM107A expression was associated with a poorer prognosis and unfavorable clinicopathological characteristics, such as degree of differentiation, T-stage, and N-stage. Overexpression of FAM107A suppressed ESCC cell proliferation, invasion, migration, the EMT process, and cell cycle progression. Finally, FAM107A overexpression inhibited tumor development in vivo. The decreased expression of FAM107A is indicative of a worse prognosis for ESCC patients. FAM107A exerts inhibitory impacts on malignant behavior and may hold promise as a therapeutic target for ESCC.

Sections du résumé

BACKGROUND BACKGROUND
Sequence similarity Family 107 member A (FAM107A) has been recognized as a tumor suppressor of various malignancies, which suppresses tumor proliferation and metastasis. Its specific role in esophageal squamous cell carcinoma (ESCC) remains unclear.
METHODS METHODS
Public datasets including Gene Expression Profiling Interactive Analysis (GEPIA) and Gene Expression Omnibus (GEO), quantitative real-time PCR (qRT-PCR), and Western blot were utilized for comparative analysis of FAM107A expression between ESCC and normal tissues. The link between FAM107A and clinicopathological features, as well as prognosis determined through χ2-test, log-rank analysis, and univariate and multivariate analyses, respectively. The impact of FAM107A on ESCC cell malignant behavior was confirmed through in vitro assays, including cell counting using the Cell Counting Kit-8 (CCK-8), clonal formation, wound healing, and transwell assays. Western blot analysis was employed to assess the effects of FAM107A on tumor epithelial-mesenchymal transition (EMT) and cell cycle-related proteins. Finally, xenograft tumors were developed to investigate the influence of FAM107A on ESCC growth in vivo.
RESULTS RESULTS
FAM107A exhibited low expression in ESCC tissues. Reduced FAM107A expression was associated with a poorer prognosis and unfavorable clinicopathological characteristics, such as degree of differentiation, T-stage, and N-stage. Overexpression of FAM107A suppressed ESCC cell proliferation, invasion, migration, the EMT process, and cell cycle progression. Finally, FAM107A overexpression inhibited tumor development in vivo.
CONCLUSION CONCLUSIONS
The decreased expression of FAM107A is indicative of a worse prognosis for ESCC patients. FAM107A exerts inhibitory impacts on malignant behavior and may hold promise as a therapeutic target for ESCC.

Identifiants

pubmed: 37977035
pii: S0344-0338(23)00646-5
doi: 10.1016/j.prp.2023.154945
pii:
doi:

Substances chimiques

Cell Cycle Proteins 0
FAM107A protein, human 0
Nuclear Proteins 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

154945

Informations de copyright

Copyright © 2023 Elsevier GmbH. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declare that they have no conflict of interest.

Auteurs

Jiale Zhang (J)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China.

Shouyin Di (S)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China.

Mingyang Li (M)

State Key Laboratory of Cancer Biology, Department of Pathology, Xijing Hospital and School of Basic Medicine, Fourth Military Medical University, Xi'an, China.

Yanxin Dong (Y)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China.

Shun Xie (S)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China.

Taiqian Gong (T)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China. Electronic address: gongtq_thoracic@163.com.

Peizhen Hu (P)

State Key Laboratory of Cancer Biology, Department of Pathology, Xijing Hospital and School of Basic Medicine, Fourth Military Medical University, Xi'an, China. Electronic address: hupigeon@163.com.

Qingge Jia (Q)

Department of Reproductive Medicine, Xi'an International Medical Center Hospital, Northwest University, Xi'an, China. Electronic address: 361400283@qq.com.

Boshi Fan (B)

Department of Thoracic Surgery, The Sixth Medical Center of PLA General Hospital of Beijing, Beijing, China. Electronic address: boshifan@yeah.net.

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