Downregulation of long non‑coding RNA GACAT1 suppresses proliferation and induces apoptosis of NSCLC cells by sponging microRNA‑422a
Increasing evidence has demonstrated the important roles of long non‑coding (lnc) RNA in non‑small cell lung cancer (NSCLC). lncRNA gastric cancer‑associated transcript 1 (GACAT1) has been reported to play an oncogenic role in different types of cancer; however, the function of GACAT1 in NSCLC remai...
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| Veröffentlicht in: | International journal of molecular medicine 2021-02, Vol.47 (2), p.659-667 |
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| creator | Zhong, Youqing Lin, Hui Li, Qi Liu, Chang Zhong, Lei |
| description | Increasing evidence has demonstrated the important roles of long non‑coding (lnc) RNA in non‑small cell lung cancer (NSCLC). lncRNA gastric cancer‑associated transcript 1 (GACAT1) has been reported to play an oncogenic role in different types of cancer; however, the function of GACAT1 in NSCLC remains unclear. The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)‑422a mechanically and negatively regulated miR‑422a expression. Reduced expression of miR‑422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR‑422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR‑422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. Taken together, these results revealed the novel role of the GACAT1/miR‑422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment. |
| doi_str_mv | 10.3892/ijmm.2020.4826 |
| format | Article |
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The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)‑422a mechanically and negatively regulated miR‑422a expression. Reduced expression of miR‑422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR‑422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR‑422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. Taken together, these results revealed the novel role of the GACAT1/miR‑422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment.</description><identifier>ISSN: 1107-3756</identifier><identifier>EISSN: 1791-244X</identifier><identifier>DOI: 10.3892/ijmm.2020.4826</identifier><identifier>PMID: 33416153</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Apoptosis ; Binding sites ; Biotechnology ; Cancer therapies ; Cell cycle ; Chemotherapy ; Experiments ; Gastric cancer ; Gene expression ; Health aspects ; Instrument industry ; Lung cancer ; Lung cancer, Non-small cell ; Lymphatic system ; Medical prognosis ; Metastasis ; MicroRNA ; MicroRNAs ; Proteins ; Scientific equipment and supplies industry ; Stomach cancer ; Surgery</subject><ispartof>International journal of molecular medicine, 2021-02, Vol.47 (2), p.659-667</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Zhong et al. 2021</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-21b9b370fa309ac862fbebaa71efd4a7e7fcbf9e33e083289fa77925b40194013</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33416153$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhong, Youqing</creatorcontrib><creatorcontrib>Lin, Hui</creatorcontrib><creatorcontrib>Li, Qi</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><creatorcontrib>Zhong, Lei</creatorcontrib><title>Downregulation of long non‑coding RNA GACAT1 suppresses proliferation and induces apoptosis of NSCLC cells by sponging microRNA‑422a</title><title>International journal of molecular medicine</title><addtitle>Int J Mol Med</addtitle><description>Increasing evidence has demonstrated the important roles of long non‑coding (lnc) RNA in non‑small cell lung cancer (NSCLC). lncRNA gastric cancer‑associated transcript 1 (GACAT1) has been reported to play an oncogenic role in different types of cancer; however, the function of GACAT1 in NSCLC remains unclear. The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)‑422a mechanically and negatively regulated miR‑422a expression. Reduced expression of miR‑422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR‑422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR‑422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. Taken together, these results revealed the novel role of the GACAT1/miR‑422a pathway in the progression of NSCLC cell lines, providing a possible therapeutic strategy for NSCLC treatment.</description><subject>Apoptosis</subject><subject>Binding sites</subject><subject>Biotechnology</subject><subject>Cancer therapies</subject><subject>Cell cycle</subject><subject>Chemotherapy</subject><subject>Experiments</subject><subject>Gastric cancer</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>Instrument industry</subject><subject>Lung cancer</subject><subject>Lung cancer, Non-small cell</subject><subject>Lymphatic system</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>Proteins</subject><subject>Scientific equipment and supplies industry</subject><subject>Stomach cancer</subject><subject>Surgery</subject><issn>1107-3756</issn><issn>1791-244X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNptkstu1TAQhiMEoqWwZYkssc6pb4mTDVKUQkE6KlIpEjvLceyDjxI72Amouy675RV5EibqBSrVluXLzHwzHv1Z9prgDatqeuz247ihmOINr2j5JDskoiY55fzbUzgTLHImivIge5HSHmNa8Lp6nh0wxklJCnaYXZ-EXz6a3TKo2QWPgkVD8Dvkg_9z9VuH3sHl_KxBp03bXBCUlmmKJiWT0BTD4KyJN4HK98j5ftFgUVOY5pBcWnFnX9pti7QZhoS6S5QmwK_Q0ekYgAxpOKXqZfbMqiGZV7f7Ufb1w_uL9mO-_Xz6qW22ueZVMeeUdHXHBLaK4VrpqqS2M51SghjbcyWMsLqztWHM4IrRqrZKiJoWHcekhsWOsnc33GnpRtNr4-eoBjlFN6p4KYNy8qHFu-9yF35KwAhOCwC8vQXE8GMxaZb7sEQPNUvKheAYEol_Xjs1GOm8DQDTo0taNmWBYVDCwGvziBfM3kB7gjfWwftjAdC7lKKx94UTLFdByFUQchWEXAUBAW_-_-69-50C2F9TFbQb</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Zhong, Youqing</creator><creator>Lin, Hui</creator><creator>Li, Qi</creator><creator>Liu, Chang</creator><creator>Zhong, Lei</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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The present study found that GACAT1 was overexpressed in NSCLC tissues and was associated with poor outcomes in patients with NSCLC. Functional experiments revealed that GACAT1 downregulation inhibited proliferation, induced apoptosis and cell cycle arrest of 2 NSCLC cell lines. GACAT1 was found to target microRNA(miR)‑422a mechanically and negatively regulated miR‑422a expression. Reduced expression of miR‑422a in NSCLC tissues was inversely correlated with that of GACAT1. Furthermore, YY1 transcription factor (YY1) was identified as a downstream miR‑422a target. Reduced expression of GACAT1 inactivated YY1 by sponging miR‑422a in NSCLC cells. YY1 reintroduction reversed the reduced proliferation of NSCLC cells via GACAT1 knockdown. 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| source | Spandidos Publications Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Apoptosis Binding sites Biotechnology Cancer therapies Cell cycle Chemotherapy Experiments Gastric cancer Gene expression Health aspects Instrument industry Lung cancer Lung cancer, Non-small cell Lymphatic system Medical prognosis Metastasis MicroRNA MicroRNAs Proteins Scientific equipment and supplies industry Stomach cancer Surgery |
| title | Downregulation of long non‑coding RNA GACAT1 suppresses proliferation and induces apoptosis of NSCLC cells by sponging microRNA‑422a |
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