Aloe-Emodin Isolated from Rheum Undulatum L. Regulates Cell Cycle Distribution and Cellular Senescence in Human Prostate Cancer LNCaP Cells

Abstract

Senescence can promote hyperplastic pathologies, such as cancer. Prostate cancer is the second most common type of cancer in men. The p21-mediate cellular senescence, facilitated through the tumor suppressor p53-dependent pathway, is considered the primary mechanism for cancer treatment. Aloe-emodin, has been reported to exert anticancer effects in various types of cancers. This study aimed to investigate the bioactivity of aloe-emodin in LNCaP cells via the activation of p21-mediated cellular senescence. Aloe-emodin treatment increased the percentage of cells in the G1 phase while decreasing the percentage in the S phase. This effect was reflected in the expression levels of proteins associated with cell cycle progression, such as p21CIP, retinoblastoma protein, and cyclin-dependent kinase2/4 in LNCaP cells. However, aloe-emodin-treated LNCaP cells did not induce cell cycle arrest at G2/M checkpoint. Moreover, increased senescence-associated-galactosidase activity was observed in a dose-dependent manner following treatment with aloe-emodin. Aloe-emodin also induced DNA damage by modulating the expression of histone H2AX and lamin B1. Furthermore, aloe-emodin inhibited the proliferation of LNCaP cells, contrasting with the exponential growth observed in the nontreated cells. Importantly, this inhibition did not impact the immune system, as evidenced by the increased proliferation of splenocytes isolated from mice. These findings provide preliminary evidence of the anticancer effect of aloe-emodin in LNCaP cells, necessitating further investigations into the underlying mechanisms in vivo and human subjects.

Keywords:

• aloe-emodin
• cell cycle arrest
• LNCaP cell
• prostate cancer
• senescence

Disclosure statement

The authors declare that they have no competing financial interests or personal relationships that may have influenced the work reported in this study.

Data availability statement

Data will be made available on request.

Correction Statement

This article has been corrected with minor changes. These changes do not impact the academic content of the article.

Additional information

Funding

This research was supported by the Korea Institute of Science and Technology (KIST) Institutional Program (2E32641-23-058).

Notes on contributors

Mei Tong He

Mei Tong He, PhD., Researcher at College of Korean Medicine, Gachon University, Republic of Korea.

Quynh Nhu Nguyen

Quynh Nhu Nguyen, Master of Chinese Medicine, Doctoral Researcher in Experimental and Clinical Medicine in Hematology and Oncology, University Hospital Ostrava, Czech Republic.

Eun Ju Cho

Eun Ju Cho, PhD, Researcher at Department of Food Science & Nutrition, Pusan National University, Republic of Korea.

Seung Hyun Kim

Seung Hyun Kim, PhD, College of Pharmacy, Yonsei Institute of Pharmaceutical Sciences, Yonsei University, Republic of Korea.

SeonJu Park

SeonJu Park, PhD, Chuncheon Center, Korea Basic Science Institute (KBSI), Republic of Korea.

Jun Yeon Park

Jun Yeon Park, PhD, Department of Food Science and Biotechnology, Kyonggi University, Republic of Korea.

Sullim Lee

Sullim Lee, PhD, Department of Life Science, College of Bio-Nano Technology, Gachon University, Republic of Korea.

Ki Sung Kang

Ki Sung Kang, PhD, College of Korean Medicine, Gachon University, Republic of Korea.