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Updated: Feb 5, 2026

Multidimensional Coculture System to Model Lung Squamous Carcinoma Progression
Published on: March 17, 2020
Loss of UHRF2 Is Associated With Non-small Cell Lung Carcinoma Progression
Chun Jin1, Dian Xiong2, Hao-Ran Li1
1Department of Thoracic Surgery, The Affiliated Zhongshan Hospital of Fudan University, Shanghai 200032, P. R. China.
Abstract:
Recent evidence indicated ubiquitin like with PHD and ring finger domains 2 (UHRF2) was involved in various human diseases, especially in cancer, however, its roles in cancer are still in dispute. Here, we found UHRF2 expression was decreased in lung cancer tissues compared with adjacent normal tissues by referring to the Oncomine Database, which was further identified by immunoblotting and quantitative real-time polymerase chain reaction assays. Secondly, we found knockdown of UHRF2 in A549 and 95-D cell lines enhanced the capability of proliferation, invasion and migration, while forced UHRF2 expression inhibited NSCLC cells proliferation,invasion and migration. Mechanistically, dot-blot and western blot assays indicated that the level of UHRF2 was positively correlated with 5-hmC level by affecting ten-eleven translocation 2 (TET2) expression. Clinically, UHRF2 downregulation is significantly correlated with a malignant phenotype, including larger tumor size and poor differentiation. Moreover, UHRF2 downregulated correlates with shorter overall survival(OS). Conclusion: Our findings indicate that UHRF2 is a tumor suppressor in NSCLC by influence TET2 expression and serve as a potential therapeutic target in NSCLC.
Insights
Ubiquitin like with PHD and ring finger domains 2 (UHRF2) acts as a tumor suppressor in non-small cell lung cancer (NSCLC). Decreased UHRF2 expression promotes cancer progression and is linked to poorer patient survival.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Ubiquitin like with PHD and ring finger domains 2 (UHRF2) has been implicated in human diseases, but its specific role in cancer remains unclear.
- Existing research presents conflicting evidence regarding the function of UHRF2 in oncogenesis.
Purpose of the Study:
- To investigate the role of UHRF2 in non-small cell lung cancer (NSCLC).
- To explore the molecular mechanisms underlying UHRF2's function in NSCLC.
- To evaluate the clinical significance of UHRF2 expression in NSCLC patients.
Main Methods:
- Analysis of UHRF2 expression in lung cancer tissues using the Oncomine Database.
- Experimental validation of UHRF2 expression via immunoblotting and quantitative real-time polymerase chain reaction (qRT-PCR).
- In vitro studies involving UHRF2 knockdown and overexpression in NSCLC cell lines (A549, 95-D).
- Assays to assess the correlation between UHRF2, ten-eleven translocation 2 (TET2) expression, and 5-hydroxymethylcytosine (5-hmC) levels.
Main Results:
- UHRF2 expression was significantly decreased in lung cancer tissues compared to normal tissues.
- Knockdown of UHRF2 promoted proliferation, invasion, and migration of NSCLC cells, while its overexpression inhibited these processes.
- UHRF2 expression positively correlated with TET2 expression and 5-hmC levels.
- Downregulation of UHRF2 was associated with advanced tumor characteristics (larger size, poor differentiation) and shorter overall survival in NSCLC patients.
Conclusions:
- UHRF2 functions as a tumor suppressor in NSCLC.
- UHRF2 exerts its tumor-suppressive effects possibly through the regulation of TET2 expression, impacting 5-hmC levels.
- UHRF2 represents a potential therapeutic target for NSCLC treatment.
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