Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway
Abstract Background Epiplakin1 (EPPK1) has been associated with disease progression and unfavorable prognosis of many cancers, but its functional involvement in esophageal squamous cell carcinoma (ESCC) remains to be uncovered. Methods The Quantitative Real‐time PCR (qPCR) assay was employed to dete...
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2022-04-01
|
| Series: | Thoracic Cancer |
| Subjects: | |
| Online Access: | https://doi.org/10.1111/1759-7714.14366 |
| _version_ | 1818271870122721280 |
|---|---|
| author | Zhongshi Qiao Chengcheng Dai Zhiqian Wang Zifan Wang Zheng Wang Tongsong Zhang Wenjing Niu Xuezhen Ma |
| author_facet | Zhongshi Qiao Chengcheng Dai Zhiqian Wang Zifan Wang Zheng Wang Tongsong Zhang Wenjing Niu Xuezhen Ma |
| author_sort | Zhongshi Qiao |
| collection | DOAJ |
| description | Abstract Background Epiplakin1 (EPPK1) has been associated with disease progression and unfavorable prognosis of many cancers, but its functional involvement in esophageal squamous cell carcinoma (ESCC) remains to be uncovered. Methods The Quantitative Real‐time PCR (qPCR) assay was employed to determine the expression of EPPK1 in ESCC tissues and cells. CCK‐8 assay, colony forming assay, wound healing assay, and transwell invasion assay were utilized to evaluate the effects of EPPK1 on cell proliferation, migration, and invasion capacity in ESCC cells using small interfering ribonucleic acids. Flow cytometry was performed to estimate the cell apoptotic rate caused by silencing of EPPK1. The proteins related to epithelial‐to‐mesenchymal transition (EMT), apoptosis, and activation of the phosphatidylinositol 3‐kinase/serine threonine protein kinase 1 (PI3K/AKT) signaling pathway were measured by western blot. Results The expression of EPPK1 was dramatically increased in ESCC tissues and cells compared to that in relative controls. Additionally, silencing of EPPK1 suppressed ESCC cell growth, colony formation, migration, invasion, and EMT, while promoting ESCC cell apoptosis. Furthermore, EPPK1 induced ESCC cell progression via mediating the PI3K/AKT signaling pathway. Conclusion EPPK1 promotes ESCC progression by modulating the PI3K/AKT signaling pathway and could serve as a potential target for ESCC treatment. |
| first_indexed | 2024-12-12T21:33:02Z |
| format | Article |
| id | doaj.art-e0cc5d36864f49e1a1fffcd199bb2941 |
| institution | Directory Open Access Journal |
| issn | 1759-7706 1759-7714 |
| language | English |
| last_indexed | 2024-12-12T21:33:02Z |
| publishDate | 2022-04-01 |
| publisher | Wiley |
| record_format | Article |
| series | Thoracic Cancer |
| spelling | doaj.art-e0cc5d36864f49e1a1fffcd199bb29412022-12-22T00:11:16ZengWileyThoracic Cancer1759-77061759-77142022-04-011381117112510.1111/1759-7714.14366Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathwayZhongshi Qiao0Chengcheng Dai1Zhiqian Wang2Zifan Wang3Zheng Wang4Tongsong Zhang5Wenjing Niu6Xuezhen Ma7Cancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaCancer Center, The Affiliated Qingdao Central Hospital of Qingdao University The Second Affiliated Hospital of Medical College of Qingdao University Qingdao Shandong ChinaAbstract Background Epiplakin1 (EPPK1) has been associated with disease progression and unfavorable prognosis of many cancers, but its functional involvement in esophageal squamous cell carcinoma (ESCC) remains to be uncovered. Methods The Quantitative Real‐time PCR (qPCR) assay was employed to determine the expression of EPPK1 in ESCC tissues and cells. CCK‐8 assay, colony forming assay, wound healing assay, and transwell invasion assay were utilized to evaluate the effects of EPPK1 on cell proliferation, migration, and invasion capacity in ESCC cells using small interfering ribonucleic acids. Flow cytometry was performed to estimate the cell apoptotic rate caused by silencing of EPPK1. The proteins related to epithelial‐to‐mesenchymal transition (EMT), apoptosis, and activation of the phosphatidylinositol 3‐kinase/serine threonine protein kinase 1 (PI3K/AKT) signaling pathway were measured by western blot. Results The expression of EPPK1 was dramatically increased in ESCC tissues and cells compared to that in relative controls. Additionally, silencing of EPPK1 suppressed ESCC cell growth, colony formation, migration, invasion, and EMT, while promoting ESCC cell apoptosis. Furthermore, EPPK1 induced ESCC cell progression via mediating the PI3K/AKT signaling pathway. Conclusion EPPK1 promotes ESCC progression by modulating the PI3K/AKT signaling pathway and could serve as a potential target for ESCC treatment.https://doi.org/10.1111/1759-7714.14366EPPK1ESCCPI3K/AKT pathwaytumor progression |
| spellingShingle | Zhongshi Qiao Chengcheng Dai Zhiqian Wang Zifan Wang Zheng Wang Tongsong Zhang Wenjing Niu Xuezhen Ma Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway Thoracic Cancer EPPK1 ESCC PI3K/AKT pathway tumor progression |
| title | Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway |
| title_full | Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway |
| title_fullStr | Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway |
| title_full_unstemmed | Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway |
| title_short | Epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the PI3K‐AKT signaling pathway |
| title_sort | epiplakin1 promotes the progression of esophageal squamous cell carcinoma by activating the pi3k akt signaling pathway |
| topic | EPPK1 ESCC PI3K/AKT pathway tumor progression |
| url | https://doi.org/10.1111/1759-7714.14366 |
| work_keys_str_mv | AT zhongshiqiao epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT chengchengdai epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT zhiqianwang epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT zifanwang epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT zhengwang epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT tongsongzhang epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT wenjingniu epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway AT xuezhenma epiplakin1promotestheprogressionofesophagealsquamouscellcarcinomabyactivatingthepi3kaktsignalingpathway |