Int J Biol Sci 2022; 18(1):214-228. doi:10.7150/ijbs.65654 This issue

Research Paper

PPDPF Promotes the Progression and acts as an Antiapoptotic Protein in Non-Small Cell Lung Cancer

Mu Yun1,3, Li Yingzi2, Gao Jie1,3,4,5, Liu Guanxin2, Zeng Zimei1,3,4,5, Cao Zhen1,3,4,5, Li Zhi1,3,4,5, Nie Yingjie6, Sun Lunquan1,3,4,5✉, Chen Tao2✉, Deng Yuezhen1,3,4,5✉, Zhou Chengzhi2✉

1. Department of Oncology, Xiangya Cancer Center, Xiangya Hospital, Central South University, Changsha 410008, China.
2. State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou 510120, China.
3. Key Laboratory of Molecular Radiation Oncology Hunan Province, Changsha 410008, China.
4. Hunan International Science and Technology Collaboration Base of Precision Medicine for Cancer, Changsha 410008, China.
5. Center for Molecular Imaging of Central South University, Xiangya Hospital, Changsha 410008, China.
6. NHC Key Laboratory of Pulmonary Immune-related Diseases, Guizhou Provincial People's Hospital; Guiyang 550000, China.

This is an open access article distributed under the terms of the Creative Commons Attribution License ( See for full terms and conditions.
Yun M, Yingzi L, Jie G, Guanxin L, Zimei Z, Zhen C, Zhi L, Yingjie N, Lunquan S, Tao C, Yuezhen D, Chengzhi Z. PPDPF Promotes the Progression and acts as an Antiapoptotic Protein in Non-Small Cell Lung Cancer. Int J Biol Sci 2022; 18(1):214-228. doi:10.7150/ijbs.65654. Available from

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Graphic abstract

Resistance to radiotherapy is frequently observed in the clinic and leads to poor prognosis of non-small cell lung cancer (NSCLC). How to overcome resistance to radiotherapy is a challenge in the treatment of NSCLC. In this study, PPDPF was found to be upregulated in NSCLC tissues and cell lines, and its expression negatively correlated with the overall survival of patients with NSCLC. PPDPF promoted the growth, colony formation and invasion of lung cancer cells. Moreover, knockout of PPDPF inhibited tumorigenesis in the KL (KrasG12D; LKB1f/f) mouse model of lung cancer. Additionally, overexpression of PPDPF led to radioresistance in lung cancer cells, and knockdown of PPDPF sensitized lung cancer cells to radiotherapy. Mechanistically, PPDPF interacted with BABAM2 (an antiapoptotic protein) and blocked its ubiquitination by MDM2, thus stabilizing BABAM2 and promoting the radioresistance of lung cancer cells. Our present study suggested PPDPF as a therapeutic target in NSCLC.

Keywords: PPDPF, NSCLC, BABAM2, MDM2, radioresistance