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Published on: January 19, 2019
Overexpression of PTPRCAP inhibits biological function of lung adenocarcinoma through apoptosis pathway
Yuting Yang1, Baoshan Zhao1, Yingjie Jiang1
1Department of Thoracic Surgery, Affiliated Hospital of Chengde Medical University, Chengde, Hebei Province, China.
Background:
PTPRCAP (protein tyrosine phosphatase receptor C-associated protein) has been implicated in tumor suppression in several malignancies; however, its role in lung adenocarcinoma (LUAD) remains unclear. This study aimed to investigate the expression profile and functional significance of PTPRCAP in LUAD.
Methods:
Forty-five pairs of LUAD and adjacent non-tumor tissues were collected from patients undergoing surgery at Chengde Medical University Affiliated Hospital. PTPRCAP mRNA and protein levels were quantified by RT-qPCR and immunohistochemistry (IHC), respectively, and correlated with clinicopathological features. A549 and H1299 LUAD cell lines and BEAS-2B normal bronchial epithelial cells were used for in vitro assays. PTPRCAP was overexpressed via plasmid transfection (OE group) and compared with vector-transfected controls (Vector group). Functional assays included CCK-8 proliferation, scratch wound healing, Transwell migration/invasion, and Annexin V-PE apoptosis assays. Apoptosis-related proteins (Bax, Bcl-2, and cleaved caspase-3) were evaluated by Western blot. The effect of overexpression PTPRCAP on tumor growth was observed through nude mouse xenografts.
Results:
PTPRCAP mRNA and protein levels were significantly lower in LUAD tissues than in adjacent non-tumor tissues (P < 0.05). Low PTPRCAP expression correlated with advanced TNM stage and poor differentiation (P < 0.05). In vitro, PTPRCAP expression was markedly reduced in A549 and H1299 cells compared with BEAS-2B. Overexpression of PTPRCAP significantly suppressed proliferation, migration, and invasion (P < 0.001), and increased apoptosis rates in both cell lines (P < 0.01). Mechanistically, PTPRCAP upregulation elevated pro-apoptotic Bax and cleaved caspase-3 while downregulating anti-apoptotic Bcl-2 (P < 0.05). In vivo xenograft experiments demonstrated that overexpression PTPRCAP inhibited tumor growth in nude mice (P < 0.001).
Conclusions:
PTPRCAP is downregulated in LUAD and acts as a tumor suppressor by promoting apoptosis and inhibiting proliferation, migration, and invasion. These findings suggest PTPRCAP as a potential therapeutic target for LUAD.
Insights
Protein tyrosine phosphatase receptor C-associated protein (PTPRCAP) is downregulated in lung adenocarcinoma (LUAD), acting as a tumor suppressor. Its restoration inhibits LUAD cell proliferation, migration, and invasion, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Protein tyrosine phosphatase receptor C-associated protein (PTPRCAP) is a known tumor suppressor in various cancers.
- Its specific role and expression in lung adenocarcinoma (LUAD) remain largely uncharacterized.
- Understanding PTPRCAP's function in LUAD is crucial for developing novel therapeutic strategies.
Purpose of the Study:
- To investigate the expression profile of PTPRCAP in LUAD tissues and cell lines.
- To elucidate the functional significance of PTPRCAP in LUAD progression.
- To evaluate PTPRCAP as a potential therapeutic target for LUAD.
Main Methods:
- Quantitative analysis of PTPRCAP mRNA and protein levels in LUAD tissues and cell lines using RT-qPCR and immunohistochemistry.
- In vitro functional assays including proliferation, migration, invasion, and apoptosis assays following PTPRCAP overexpression.
- Western blot analysis of apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-3).
- In vivo assessment of PTPRCAP's effect on tumor growth using nude mouse xenograft models.
Main Results:
- PTPRCAP expression was significantly downregulated in LUAD tissues and cell lines compared to normal controls.
- Low PTPRCAP levels correlated with advanced TNM stage and poor tumor differentiation.
- Overexpression of PTPRCAP suppressed LUAD cell proliferation, migration, and invasion, while promoting apoptosis.
- PTPRCAP upregulation modulated apoptosis-related proteins, increasing Bax and cleaved caspase-3 and decreasing Bcl-2.
- In vivo studies confirmed that PTPRCAP overexpression inhibited tumor growth.
Conclusions:
- PTPRCAP functions as a tumor suppressor in LUAD by inhibiting proliferation, migration, and invasion, and promoting apoptosis.
- The downregulation of PTPRCAP is a significant event in LUAD development.
- PTPRCAP represents a promising therapeutic target for LUAD treatment.
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