Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression
Abstract Invasiveness of pituitary adenoma is the main cause of its poor prognosis, mechanism of which remains largely unknown. In this study, the differential proteins between invasive and non-invasive pituitary tumors (IPA and NIPA) were identified by TMT labeled quantitative proteomics. The diffe...
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BMC
2025-01-01
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| Series: | Cancer & Metabolism |
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| Online Access: | https://doi.org/10.1186/s40170-024-00372-0 |
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| author | Tongjiang Xu Xiaodong Zhai RuiWei Wang Xiaoben Wu ZhiZhen Zhou MiaoMiao Shang Chongcheng Wang Tengfei Qi Wei Yang |
| author_facet | Tongjiang Xu Xiaodong Zhai RuiWei Wang Xiaoben Wu ZhiZhen Zhou MiaoMiao Shang Chongcheng Wang Tengfei Qi Wei Yang |
| author_sort | Tongjiang Xu |
| collection | DOAJ |
| description | Abstract Invasiveness of pituitary adenoma is the main cause of its poor prognosis, mechanism of which remains largely unknown. In this study, the differential proteins between invasive and non-invasive pituitary tumors (IPA and NIPA) were identified by TMT labeled quantitative proteomics. The differential metabolites in venous bloods from patients with IPA and NIPA were analyzed by untargeted metabolomics. Proteomic data showed that the top five up-regulated proteins were AD021, C2orf15, PLCXD3, HIST3H2BB and POU1F1, and the top five down-regulated proteins were AIPL1, CALB2, GLUD2, SLC4A10 and GTF2I. Metabolomic data showed that phosphatidylinositol (PI) was most remarkably up-regulated and melibiose was most obviously down-regulated. Further investigation demonstrated that PI stimulation increased the expression of PITPNM1, POU1F1, C2orf15 and LDHA as well as the phosphorylation of AKT and ERK, and promoted the proliferation, migration and invasion of GH3 cells, which were blocked by PITPNM1knockdown. Inhibiting AKT phosphorylation reduced the expression of POU1F1, C2orf15 and LDHA in PI-stimulated cells while activating AKT increased their expression in PITPNM1-silencing cells, which was similar to the function of ERK. POU1F1 silence suppressed the expression of LDHA and C2orf15. Luciferase report assay and ChIP assay demonstrated that POU1F1 positively regulated the transcription of LDHA and C2orf15. In addition, PI propelled the metastasis of GH3 cells in vivo, and elevated the expression of PITPNM1, POU1F1, C2orf15 and LDHA. These results suggested that elevated serum PI might contribute to the proliferation and invasion of pituitary adenoma by regulating the expression of PITPNM1/AKT/ERK/POU1F1 axis. |
| format | Article |
| id | doaj-art-a4951bfd3d0b4e9a9f1c97cffc5ea4ff |
| institution | Kabale University |
| issn | 2049-3002 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | BMC |
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| series | Cancer & Metabolism |
| spelling | doaj-art-a4951bfd3d0b4e9a9f1c97cffc5ea4ff2025-01-19T12:36:36ZengBMCCancer & Metabolism2049-30022025-01-0113111410.1186/s40170-024-00372-0Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expressionTongjiang Xu0Xiaodong Zhai1RuiWei Wang2Xiaoben Wu3ZhiZhen Zhou4MiaoMiao Shang5Chongcheng Wang6Tengfei Qi7Wei Yang8Department of Neurosurgery, Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Neurosurgery, Provincial Hospital Affiliated to Shandong First Medical UniversityDepartment of Anesthesiology, Provincial Hospital affiliated to Shandong First Medical UniversityDepartment of Clinical Laboratory, Provincial Hospital affiliated to Shandong First Medical UniversityDepartment of Neurosurgery, Weishan People’s HospitalDepartment of Neurosurgery, Provincial Hospital Affiliated to Shandong First Medical UniversityTrauma Center, Provincial Hospital Affiliated to Shandong First Medical University, Jinan Trauma Center, Provincial Hospital Affiliated to Shandong First Medical University, Jinan Department of Neurosurgery, Provincial Hospital Affiliated to Shandong First Medical UniversityAbstract Invasiveness of pituitary adenoma is the main cause of its poor prognosis, mechanism of which remains largely unknown. In this study, the differential proteins between invasive and non-invasive pituitary tumors (IPA and NIPA) were identified by TMT labeled quantitative proteomics. The differential metabolites in venous bloods from patients with IPA and NIPA were analyzed by untargeted metabolomics. Proteomic data showed that the top five up-regulated proteins were AD021, C2orf15, PLCXD3, HIST3H2BB and POU1F1, and the top five down-regulated proteins were AIPL1, CALB2, GLUD2, SLC4A10 and GTF2I. Metabolomic data showed that phosphatidylinositol (PI) was most remarkably up-regulated and melibiose was most obviously down-regulated. Further investigation demonstrated that PI stimulation increased the expression of PITPNM1, POU1F1, C2orf15 and LDHA as well as the phosphorylation of AKT and ERK, and promoted the proliferation, migration and invasion of GH3 cells, which were blocked by PITPNM1knockdown. Inhibiting AKT phosphorylation reduced the expression of POU1F1, C2orf15 and LDHA in PI-stimulated cells while activating AKT increased their expression in PITPNM1-silencing cells, which was similar to the function of ERK. POU1F1 silence suppressed the expression of LDHA and C2orf15. Luciferase report assay and ChIP assay demonstrated that POU1F1 positively regulated the transcription of LDHA and C2orf15. In addition, PI propelled the metastasis of GH3 cells in vivo, and elevated the expression of PITPNM1, POU1F1, C2orf15 and LDHA. These results suggested that elevated serum PI might contribute to the proliferation and invasion of pituitary adenoma by regulating the expression of PITPNM1/AKT/ERK/POU1F1 axis.https://doi.org/10.1186/s40170-024-00372-0MetabolomicPhosphatidylinositolPITPNM1Pituitary tumorPOU1F1Proteomic |
| spellingShingle | Tongjiang Xu Xiaodong Zhai RuiWei Wang Xiaoben Wu ZhiZhen Zhou MiaoMiao Shang Chongcheng Wang Tengfei Qi Wei Yang Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression Cancer & Metabolism Metabolomic Phosphatidylinositol PITPNM1 Pituitary tumor POU1F1 Proteomic |
| title | Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression |
| title_full | Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression |
| title_fullStr | Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression |
| title_full_unstemmed | Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression |
| title_short | Phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating POU1F1 expression |
| title_sort | phosphatidylinositol promoted the proliferation and invasion of pituitary adenoma cells by regulating pou1f1 expression |
| topic | Metabolomic Phosphatidylinositol PITPNM1 Pituitary tumor POU1F1 Proteomic |
| url | https://doi.org/10.1186/s40170-024-00372-0 |
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