HS-1793 inhibits cell proliferation in lung cancer by interfering with the interaction between p53 and MDM2

Chungun Lim; Peter C W Lee; Sungbo Shim; Sung-Wuk Jang

doi:10.3892/ol.2022.13410

HS-1793 inhibits cell proliferation in lung cancer by interfering with the interaction between p53 and MDM2

Oncol Lett. 2022 Jul 1;24(2):290. doi: 10.3892/ol.2022.13410. eCollection 2022 Aug.

Authors

Chungun Lim^{1

2}, Peter C W Lee^{1

2

3}, Sungbo Shim⁴, Sung-Wuk Jang^{1

2

3}

Affiliations

¹ Department of Biomedical Sciences, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
² Asan Medical Institute of Convergence Science and Technology, Asan Medical Center, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
³ Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea.
⁴ Department of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, North Chungcheong 28644, Republic of Korea.

Abstract

The transcription factor or tumor suppressor protein p53 regulates numerous cellular functions, including cell proliferation, invasion, migration, senescence and apoptosis, in various types of cancer. HS-1793 is an analog of resveratrol, which exhibits anti-cancer effects on various types of cancer, including breast, prostate, colon and renal cancer, and multiple myeloma. However, to the best of our knowledge, the role of HS-1793 in lung cancer remains to be examined. The present study aimed to investigate the anti-cancer effect of HS-1793 on lung cancer and to determine its association with p53. The results revealed that HS-1793 reduced cell proliferation in lung cancer and increased p53 stability, thereby elevating the expression levels of the target genes p21 and mouse double minute 2 homolog (MDM2). When the levels of MDM2, a negative regulator of p53, are increased under normal conditions, MDM2 binds and degrades p53; however, HS-1793 inhibited this binding, confirming that p53 protein stability was increased. In conclusion, the findings of the present study provide new evidence that HS-1793 may inhibit lung cancer proliferation by disrupting the p53-MDM2 interaction.

Keywords: HS-1793; MDM2; anti-cancer; lung cancer; p53.

Grants and funding

This research was supported by the Basic Research Program through the National Research Foundation of Korea (NRF) and funded by the MSIT (grant no. NRF-2020R1A4A1016029).