FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling
Abstract Background Fermitin family member 1 (FERMT1) is highly expressed in many tumors and acts as an oncogene. Nonetheless, the precise function of FERMT1 in non-small cell lung cancer (NSCLC) has not been clearly elucidated. Methods Bioinformatics software predicted the FERMT1 expression in NSCL...
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Format: | Article |
Language: | English |
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BMC
2024-01-01
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Series: | BMC Cancer |
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Online Access: | https://doi.org/10.1186/s12885-023-11812-3 |
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author | Bao Liu Yan Feng Naiying Xie Yang Yang Dameng Yang |
author_facet | Bao Liu Yan Feng Naiying Xie Yang Yang Dameng Yang |
author_sort | Bao Liu |
collection | DOAJ |
description | Abstract Background Fermitin family member 1 (FERMT1) is highly expressed in many tumors and acts as an oncogene. Nonetheless, the precise function of FERMT1 in non-small cell lung cancer (NSCLC) has not been clearly elucidated. Methods Bioinformatics software predicted the FERMT1 expression in NSCLC. Transwell assays facilitated the detection of NSCLC cell migration and invasion. Western blotting techniques were employed to detect the protein levels regulated by FERMT1. Results FERMT1 exhibited high expression levels in NSCLC and was linked to the patients’ poor prognosis, as determined by a variety of bioinformatics predictions combined with experimental verification. FERMT1 promoted the migration and invasion of NSCLC and regulated epithelial to mesenchymal transition (EMT) -related markers. Further studies showed that FERMT1 could up-regulate the expression level of plakophilin 3(PKP3). Further research has indicated that FERMT1 can promote cell migration and invasion via up-regulating PKP3 expression. By exploring downstream signaling pathways, we found that FERMT1 has the capability to activate the p38 mitogen-activated protein kinases (p38 MAPK) signaling pathway, and knocking down PKP3 can counteract the activation induced by FERMT1 overexpression. Conclusions FERMT1 was highly expressed in NSCLC and can activate the p38 MAPK signaling pathway through up-regulation of PKP3, thus promoting the invasion and migration of NSCLC. |
first_indexed | 2024-03-08T14:15:09Z |
format | Article |
id | doaj.art-642af9ee708549a0b4ba4df750b41172 |
institution | Directory Open Access Journal |
issn | 1471-2407 |
language | English |
last_indexed | 2024-03-08T14:15:09Z |
publishDate | 2024-01-01 |
publisher | BMC |
record_format | Article |
series | BMC Cancer |
spelling | doaj.art-642af9ee708549a0b4ba4df750b411722024-01-14T12:26:35ZengBMCBMC Cancer1471-24072024-01-0124111010.1186/s12885-023-11812-3FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signalingBao Liu0Yan Feng1Naiying Xie2Yang Yang3Dameng Yang4Department of Respiratory Medical Oncology, Harbin Medical University Cancer HospitalDepartment of Medical Oncology, Beidahuang Industry Group General HospitalDepartment of Respiratory Medical Oncology, Harbin Medical University Cancer HospitalDepartment of Respiratory Medical Oncology, Harbin Medical University Cancer HospitalDepartment of Gastrointestinal Surgery, Harbin Medical University Cancer HospitalAbstract Background Fermitin family member 1 (FERMT1) is highly expressed in many tumors and acts as an oncogene. Nonetheless, the precise function of FERMT1 in non-small cell lung cancer (NSCLC) has not been clearly elucidated. Methods Bioinformatics software predicted the FERMT1 expression in NSCLC. Transwell assays facilitated the detection of NSCLC cell migration and invasion. Western blotting techniques were employed to detect the protein levels regulated by FERMT1. Results FERMT1 exhibited high expression levels in NSCLC and was linked to the patients’ poor prognosis, as determined by a variety of bioinformatics predictions combined with experimental verification. FERMT1 promoted the migration and invasion of NSCLC and regulated epithelial to mesenchymal transition (EMT) -related markers. Further studies showed that FERMT1 could up-regulate the expression level of plakophilin 3(PKP3). Further research has indicated that FERMT1 can promote cell migration and invasion via up-regulating PKP3 expression. By exploring downstream signaling pathways, we found that FERMT1 has the capability to activate the p38 mitogen-activated protein kinases (p38 MAPK) signaling pathway, and knocking down PKP3 can counteract the activation induced by FERMT1 overexpression. Conclusions FERMT1 was highly expressed in NSCLC and can activate the p38 MAPK signaling pathway through up-regulation of PKP3, thus promoting the invasion and migration of NSCLC.https://doi.org/10.1186/s12885-023-11812-3FERMT1Invasion and migrationNSCLCPKP3p38 MAPK signaling |
spellingShingle | Bao Liu Yan Feng Naiying Xie Yang Yang Dameng Yang FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling BMC Cancer FERMT1 Invasion and migration NSCLC PKP3 p38 MAPK signaling |
title | FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling |
title_full | FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling |
title_fullStr | FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling |
title_full_unstemmed | FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling |
title_short | FERMT1 promotes cell migration and invasion in non-small cell lung cancer via regulating PKP3-mediated activation of p38 MAPK signaling |
title_sort | fermt1 promotes cell migration and invasion in non small cell lung cancer via regulating pkp3 mediated activation of p38 mapk signaling |
topic | FERMT1 Invasion and migration NSCLC PKP3 p38 MAPK signaling |
url | https://doi.org/10.1186/s12885-023-11812-3 |
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