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Tytuł pozycji:

Dual relationship between long non-coding RNAs and STAT3 signaling in different cancers: New insight to proliferation and metastasis.

Tytuł :
Dual relationship between long non-coding RNAs and STAT3 signaling in different cancers: New insight to proliferation and metastasis.
Autorzy :
Ashrafizadeh M; Faculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla 34956, Istanbul, Turkey; Sabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla 34956, Istanbul, Turkey.
Gholami MH; Faculty of Veterinary Medicine, Kazerun Branch, Islamic Azad University, Kazerun, Iran.
Mirzaei S; Department of Biology, Faculty of Science, Islamic Azad University, Science and Research Branch, Tehran, Iran.
Zabolian A; Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Haddadi A; Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Farahani MV; Young Researchers and Elite Club, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Kashani SH; Department of Life Sciences, Islamic Azad University, North Tehran Branch, Tehran, Iran.
Hushmandi K; Department of Food Hygiene and Quality Control, Division of Epidemiology & Zoonoses, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran.
Najafi M; Medical Technology Research Center, Institute of Health Technology, Kermanshah University of Medical Sciences, Kermanshah 6715847141, Iran; Radiology and Nuclear Medicine Department, School of Paramedical Sciences, Kermanshah University of Medical Sciences, Kermanshah, Iran.
Zarrabi A; Sabanci University Nanotechnology Research and Application Center (SUNUM), Tuzla 34956, Istanbul, Turkey. Electronic address: .
Ahn KS; Department of Science in Korean Medicine, Kyung Hee University, 24 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447, Republic of Korea; KHU-KIST Department of Converging Science and Technology, Kyung Hee University, Seoul 02447, Republic of Korea. Electronic address: .
Khan H; Department of Pharmacy, Abdul Wali Khan University, Mardan 23200, Pakistan. Electronic address: .
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Źródło :
Life sciences [Life Sci] 2021 Apr 01; Vol. 270, pp. 119006. Date of Electronic Publication: 2021 Jan 06.
Typ publikacji :
Journal Article; Review
Język :
English
Imprint Name(s) :
Publication: <2008->: Amsterdam : Elsevier
Original Publication: Oxford; Elmsford, N. Y. [etc.] Pergamon Press.
Contributed Indexing :
Keywords: Cancer therapy; EMT; Long non-coding RNA (lncRNA); Metastasis; Proliferation; Signal transducer and activator of transcription 3 (STAT3)
Entry Date(s) :
Date Created: 20210109 Latest Revision: 20210220
Update Code :
20210221
DOI :
10.1016/j.lfs.2020.119006
PMID :
33421521
Czasopismo naukowe
Uncontrolled growth and metastasis of cancer cells is an increasing challenge for overcoming cancer, and improving survival of patients. Complicated signaling networks account for proliferation and invasion of cancer cells that need to be elucidated for providing effective cancer therapy, and minimizing their malignancy. Long non-coding RNAs (lncRNAs) are RNA molecules with a length of more than 200 nucleotides. They participate in cellular events, and their dysregulation in a common phenomenon in different cancers. Noteworthy, lncRNAs can regulate different molecular pathways, and signal transducer and activator of transcription 3 (STAT3) is one of them. STAT3 is a tumor-promoting factors in cancers due to its role in cancer proliferation (cell cycle progression and apoptosis inhibition) and metastasis (EMT induction). LncRNAs can function as upstream mediators of STAT3 pathway, reducing/enhancing its expression. This dual relationship is of importance in affecting proliferation and metastasis of cancer cells. The response of cancer cells to therapy such as chemotherapy and radiotherapy is regulated by lncRNA/STAT3 axis. Tumor-promoting lncRNAs including NEAT1, SNHG3 and H19 induces STAT3 expression, while tumor-suppressing lncRNAs such as MEG3, PTCSC3 and NKILA down-regulate STAT3 expression. Noteworthy, upstream mediators of STAT3 such as microRNAs can be regulated by lncRNAs. These complicated signaling networks are mechanistically described in the current review.
(Copyright © 2021 Elsevier Inc. All rights reserved.)

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