Evidence map›Paper›PMID 39002015›Full record

ArticleDoklady. Biochemistry and biophysics2024

The 3,3'-dimethoxy-4,4'-dihydroxy-stilbene Triazole (STT) Inhibits Liver Cancer Cell Growth by Targeting Akt/mTOR Pathway.

Meng Sun, Jiangtao Bai, Haisong Wang, Long Zhou, Shanfeng Li

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Article in Doklady. Biochemistry and biophysics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Meng SunInterventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China.
Jiangtao BaiInterventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China.
Haisong WangInterventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China.
Long ZhouInterventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China.
Shanfeng LiInterventional Vascular Surgery, Affiliated Hospital of Hebei University, 071000, Baoding, Hebei Province, China. li_shanfeng85@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study was aimed to investigate the proliferation inhibitory ability of 3,3'-dimethoxy-4,4'-dihydroxy-stilbene triazole (STT) on SNU449 and Huh7 cells. Moreover, the mechanism associated with the suppression of liver cancer cell proliferation by STT was also studied. The results revealed that STT suppresses proliferation of SNU449 and Huh7 cells to 28 and 21%, respectively treatment with 20 µM. The clonogenic survival of SNU449 and Huh7 cells was also significantly reduced after incubation with STT compared to the control cultures. In comparison to the control, STT treatment significantly decreased the invasive potential of SNU449 cells. Treatment with STT led to a prominent suppression in p62 and increase in LC3B protein expression in SNU449 cells compared to the control cells. The STT treatment dramatically decreased p-Akt and p-mTOR protein expression in SNU449 cells. Docking study revealed that STT interacts via traditional hydrogen bonding with the glutamine, phenylalanine, leucine, serine, arginine, aspartic acid, and lysine residues of Akt protein. In summary, the current study demonstrates that STT effectively suppresses the viability of SNU449 and Huh7 liver cancer cells. Moreover, STT treatment of the liver cancer cells also significantly reduces the clonogenic survival and invasive potential of SNU449 cells. Treatment of liver cancer cells with STT increases the expression of autophagic, targets anti-autophagic protein expression and down-regulates Akt/mTOR pathway to inhibit cancer growth and proliferation. Thus, STT exhibits prominent anticancer effect and needs to be investigated further as a potential candidate for the treatment of liver cancer.

Indexed as

Cell ProliferationLiver NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionStilbenesTOR Serine-Threonine KinasesTriazolesAntineoplastic AgentsCell Line, TumorHumansMolecular Docking SimulationAntineoplastic AgentsMTOR protein, humanProto-Oncogene Proteins c-aktStilbenesTOR Serine-Threonine KinasesTriazolesAkt/mTOR pathwayAnticancerAutophagyMetastasisNatural products

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.