2. Academic Validation
  3. Notoginsenoside Ft1 induces lysosomal cell death and apoptosis by inhibiting the PI3K/AKT/mTOR pathway in hepatocellular carcinoma

Notoginsenoside Ft1 induces lysosomal cell death and apoptosis by inhibiting the PI3K/AKT/mTOR pathway in hepatocellular carcinoma

  • Biomed Pharmacother. 2025 Jul:188:118181. doi: 10.1016/j.biopha.2025.118181.
Youngsic Jeon 1,  Hyukjoon Kwon 1,  Taek Chung 2,  Young Nyun Park 3,  Su-Nam Kim 4,  Jun Yeon Park 5,  Ki Sung Kang 6,  Dong-Young Woo 7,  Taejung Kim 8,  Young-Joo Kim 9
Affiliations

Affiliations

  • 1 Institute of Natural Products, Korea Institute of Science and Technology, Republic of Korea.
  • 2 Department of Pathology, Yonsei University College of Medicine, Republic of Korea.
  • 3 Department of Pathology, Graduate School of Medical Science, Brain Korea 21 Project, Yonsei University College of Medicine, Republic of Korea.
  • 4 Institute of Natural Products, Korea Institute of Science and Technology, Republic of Korea; Natural Product Applied Science, KIST School, University of Science and Technology, Republic of Korea.
  • 5 Vital To Life Co., Ltd., Republic of Korea.
  • 6 College of Korean Medicine, Gachon University, Republic of Korea.
  • 7 Natural Product Applied Science, KIST School, University of Science and Technology, Republic of Korea.
  • 8 Institute of Natural Products, Korea Institute of Science and Technology, Republic of Korea; Natural Product Applied Science, KIST School, University of Science and Technology, Republic of Korea. Electronic address: kgsing@kist.re.kr.
  • 9 Institute of Natural Products, Korea Institute of Science and Technology, Republic of Korea. Electronic address: yjkim7801@kist.re.kr.
PMID: 40451034 DOI: 10.1016/j.biopha.2025.118181
Abstract

Notoginsenoside Ft1 (NFt1) is a bioactive compound derived from Panax notoginseng, a traditional medicinal herb that exhibits various pharmacological properties, including anti-inflammatory and Anticancer effects. However, its effects on hepatocellular carcinoma (HCC) remain poorly understood. This study sought to investigate the Anticancer effects of NFt1 and uncover its fundamental mechanisms in HCC cells. NFt1 treatment inhibited cell proliferation and promoted Apoptosis by enhancing cell death markers. Transcriptome profiling using RNA-sequencing revealed that NFt1 treatment downregulated the expression of oncogenes (e.g., FOS, BRAF, RARA, MYC, and JUND), while upregulating lysosomal cell death-related genes (e.g., CTSB, CTSD, LAMP1, LAMP2, and TPP1). These effects are associated with PI3K/Akt/mTOR inhibition and increased transcriptional activity of transcription factor EB (TFEB). NFt1 treatment induced autophagic traits by suppressing the PI3K/Akt/mTOR pathway, thereby enhancing TFEB transactivity. These findings demonstrated the therapeutic promise of NFt1 in the effective management of HCC.

Keywords

Apoptosis; Lysosomal cell death; Notoginsenoside Ft1; PI3K/AKT/mTOR pathway; TFEB.

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