LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis
Abstract Background Non-small cell lung cancer (NSCLC), the most primary lung cancer subtype, threatens human health globally. Long non-coding RNAs (lncRNAs) have been uncovered to affect multiple cancers progression. Nevertheless, the specific function of long intergenic non-protein coding RNA 1806...
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| Format: | Article |
| Language: | English |
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BMC
2022-05-01
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| Series: | Cancer Cell International |
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| Online Access: | https://doi.org/10.1186/s12935-022-02560-8 |
| _version_ | 1811254206001053696 |
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| author | Shangxiao Huang Shixiong Liang Jianfeng Huang Penghui Luo Dunchang Mo Hanlei Wang |
| author_facet | Shangxiao Huang Shixiong Liang Jianfeng Huang Penghui Luo Dunchang Mo Hanlei Wang |
| author_sort | Shangxiao Huang |
| collection | DOAJ |
| description | Abstract Background Non-small cell lung cancer (NSCLC), the most primary lung cancer subtype, threatens human health globally. Long non-coding RNAs (lncRNAs) have been uncovered to affect multiple cancers progression. Nevertheless, the specific function of long intergenic non-protein coding RNA 1806 (LINC01806) in NSCLC remains elusive. Methods RT-qPCR and western blot were involved in this study. The influence of LINC01806 on NSCLC was assessed by in vitro and in vivo assays. Via ChIP, RNA pull down, RIP, and luciferase reporter assays, the in-depth cellular mechanisms of LINC01806 in NSCLC were explored. Results LINC01806 expression was high in NSCLC cell lines. Functionally, LINC01806 knockdown impeded cell proliferation, migration, invasion, and stemness, along with tumor growth. As for its mechanism, signal transducer and activator of transcription 1 (STAT1) activated LINC01806 transcription in NSCLC. Furthermore, LINC01806 sequestered microRNA-4428 (miR-4428) to enhance notch receptor 2 (NOTCH2) expression, thus activating Notch signaling pathway. Finally, in vitro and in vivo assays jointly validated that LINC01806 exerted its function in NSCLC development via miR-4428/NOTCH2 pathway. Conclusion LINC01806 enhanced NOTCH2 expression to stimulate Notch signaling via sponging miR-4428, thereby facilitating NSCLC progression, which provided a novel mechanism for NSCLC therapeutic approaches. Graphical Abstract |
| first_indexed | 2024-04-12T17:02:44Z |
| format | Article |
| id | doaj.art-d7ad4915c4484c10a8adfcd9ee32d2f8 |
| institution | Directory Open Access Journal |
| issn | 1475-2867 |
| language | English |
| last_indexed | 2024-04-12T17:02:44Z |
| publishDate | 2022-05-01 |
| publisher | BMC |
| record_format | Article |
| series | Cancer Cell International |
| spelling | doaj.art-d7ad4915c4484c10a8adfcd9ee32d2f82022-12-22T03:24:01ZengBMCCancer Cell International1475-28672022-05-0122111510.1186/s12935-022-02560-8LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axisShangxiao Huang0Shixiong Liang1Jianfeng Huang2Penghui Luo3Dunchang Mo4Hanlei Wang5Department of Radiotherapy, The Third Affiliated Hospital of Guangxi Medical UniversityDepartment of Radiotherapy, Cancer Hospital Affiliated to Guangxi Medical UniversityDepartment of Radiotherapy, The Third Affiliated Hospital of Guangxi Medical UniversityDepartment of Radiotherapy, The Third Affiliated Hospital of Guangxi Medical UniversityDepartment of Radiotherapy, The Third Affiliated Hospital of Guangxi Medical UniversityDepartment of Radiotherapy, The Third Affiliated Hospital of Guangxi Medical UniversityAbstract Background Non-small cell lung cancer (NSCLC), the most primary lung cancer subtype, threatens human health globally. Long non-coding RNAs (lncRNAs) have been uncovered to affect multiple cancers progression. Nevertheless, the specific function of long intergenic non-protein coding RNA 1806 (LINC01806) in NSCLC remains elusive. Methods RT-qPCR and western blot were involved in this study. The influence of LINC01806 on NSCLC was assessed by in vitro and in vivo assays. Via ChIP, RNA pull down, RIP, and luciferase reporter assays, the in-depth cellular mechanisms of LINC01806 in NSCLC were explored. Results LINC01806 expression was high in NSCLC cell lines. Functionally, LINC01806 knockdown impeded cell proliferation, migration, invasion, and stemness, along with tumor growth. As for its mechanism, signal transducer and activator of transcription 1 (STAT1) activated LINC01806 transcription in NSCLC. Furthermore, LINC01806 sequestered microRNA-4428 (miR-4428) to enhance notch receptor 2 (NOTCH2) expression, thus activating Notch signaling pathway. Finally, in vitro and in vivo assays jointly validated that LINC01806 exerted its function in NSCLC development via miR-4428/NOTCH2 pathway. Conclusion LINC01806 enhanced NOTCH2 expression to stimulate Notch signaling via sponging miR-4428, thereby facilitating NSCLC progression, which provided a novel mechanism for NSCLC therapeutic approaches. Graphical Abstracthttps://doi.org/10.1186/s12935-022-02560-8Non-small cell lung cancerSTAT1LINC01806miR-4428NOTCH2 |
| spellingShingle | Shangxiao Huang Shixiong Liang Jianfeng Huang Penghui Luo Dunchang Mo Hanlei Wang LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis Cancer Cell International Non-small cell lung cancer STAT1 LINC01806 miR-4428 NOTCH2 |
| title | LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis |
| title_full | LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis |
| title_fullStr | LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis |
| title_full_unstemmed | LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis |
| title_short | LINC01806 mediated by STAT1 promotes cell proliferation, migration, invasion, and stemness in non-small cell lung cancer through Notch signaling by miR-4428/NOTCH2 axis |
| title_sort | linc01806 mediated by stat1 promotes cell proliferation migration invasion and stemness in non small cell lung cancer through notch signaling by mir 4428 notch2 axis |
| topic | Non-small cell lung cancer STAT1 LINC01806 miR-4428 NOTCH2 |
| url | https://doi.org/10.1186/s12935-022-02560-8 |
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