STAT3 in Carcinogenesis: Update from 1993 to Present

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 1466

Special Issue Editors


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Guest Editor
Department of Experimental, Diagnostic and Specialty Medicine (DIMES), University of Bologna, 40138 Bologna, Italy
Interests: cancer biology; stat3; signal transduction; chemoresistance; immunotherapy
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Guest Editor
Department of Life Sciences and Public Health, Università Cattolica del Sacro Cuore, Rome, Italy
Interests: ErbB; epidermal growth factor receptor in lung cancer; STAT3 pathways

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Guest Editor
Department of Biochemical Sciences, Universita degli Studi di Roma La Sapienza, Rome, Italy
Interests: STAT3; carcinogenesis;transduction signalling pathways; biochemistry OCPs environmental pollutants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Signal Transducer and Activator of Transcription 3 (STAT3) is a 30-year-old protein. Its history begins with a paper published on Molecular and Cellular Biology in 1993. As a pro-inflammatory transcription factor, signal transducer, and transcription activator, it was identified in 1994. STAT3 is a protein with polyhedral activities: it mediates, directly or indirectly, multiple cellular signaling pathways (cytokines of growth factors, hormones, and oxidative stress), is a key protein in the modulation of metabolism and mitochondrial activity, and is involved in the regulation of microtubules dynamics in the cellular cytoskeleton.

Its activation is crucial in various diseases as chronic inflammation, cardiovascular and metabolic disorders, and cancer. In fact, a lot of scientific publications assessed the involvement of STAT3, through both its canonical and non-canonical pathways, in all three phases of carcinogenesis: initiation, promotion, and progression. STAT3 can be considered a moonlighting protein. Its multifaceted activities are mainly ensured by post-translational modifications such as phosphorylation, acetylation, glutathionylation, etc.

This Special Issue aims to review all the scientific advances on the STAT3 protein achieved in the past 30 years focusing on current and future research on the role of the STAT3 protein, its potential inhibitors or modulators in both carcinogenesis and chemoresistance phenomenon.

Moreover, this Special Issue should provide a global and actual vision of STAT3’s cellular and biological functions. We hope that researchers in the field contribute with research articles, review articles, innovative hypotheses, or commentaries on STAT3’s activities and regulations.

Dr. Donatella Romaniello
Dr. Ilaria Marrocco
Dr. Margherita Eufemi
Guest Editors

Manuscript Submission Information

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Keywords

  • STAT3
  • carcinogenesis
  • transduction signaling pathways
  • post-translational modifications
  • interactors
  • energy and cellular metabolism
  • STAT3 inhibitors

Published Papers (1 paper)

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Research

18 pages, 17825 KiB  
Article
KDF1 Promoted Proliferation, Migration and Invasion of Lung Adenocarcinoma Cells through Activating STAT3 and AKT Pathway
by Yi-Qing Guo, Mei-Fu Gan, Jia-Qian Bao, Han-Xi Zhou, Jing Yang, Chuan-Jing Dai and Jing-Min Zheng
Biomedicines 2023, 11(12), 3194; https://doi.org/10.3390/biomedicines11123194 - 1 Dec 2023
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Abstract
KDF1 has been reported to be correlated with carcinogenesis. However, its role and mechanism are far from clear. To explore the possible role and underlying mechanism of KDF1 in lung adenocarcinoma (LUAD), we investigated KDF1 expression in LUAD tissues and the influence of [...] Read more.
KDF1 has been reported to be correlated with carcinogenesis. However, its role and mechanism are far from clear. To explore the possible role and underlying mechanism of KDF1 in lung adenocarcinoma (LUAD), we investigated KDF1 expression in LUAD tissues and the influence of KDF1 in the phenotype of LUAD cells (A549 and PC-9) as well as the underlying mechanism. Compared to non-tumor lung epithelial cells, KDF1 was upregulated in the cancer cells of the majority of LUAD patients, and its expression was correlated with tumor size. Patients with enhanced KDF1 in cancer cells (compared with paired adjacent non-neoplastic lung epithelial cells) had shorter overall survival than patients with no increased KDF1 in cancer cells. Knockdown of KDF1 inhibited the migration, proliferation and invasion of LUAD cells in vitro. And overexpression of KDF1 increased the growth of the subcutaneous tumors in mice. In terms of molecular mechanisms, overexpression of KDF1 induced the expression of AKT, p-AKT and p-STAT3. In KDF1-overexpressing A549 cells, inhibition of the STAT3 pathway decreased the level of AKT and p-AKT, whereas inhibition of the AKT pathway had no effect on the activation of STAT3. Inhibition of STAT3 or AKT pathways reversed the promoting effects of KDF1 overexpression on the LUAD cell phenotype and STAT3 inhibition appeared to have a better effect. Finally, in the cancer cells of LUAD tumor samples, the KDF1 level was observed to correlate positively with the level of p-STAT3. All these findings suggest that KDF1, which activates STAT3 and the downstream AKT pathway in LUAD, acts as a tumor-promoting factor and may represent a therapeutic target. Full article
(This article belongs to the Special Issue STAT3 in Carcinogenesis: Update from 1993 to Present)
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