Salidroside inhibited the proliferation of gastric cancer cells through up-regulating tumor suppressor miR-1343-3p and down-regulating MAP3K6/MMP24 signal molecules

Cancer Biol Ther. 2024 Dec 31;25(1):2322206. doi: 10.1080/15384047.2024.2322206. Epub 2024 Mar 4.

Abstract

Salidroside inhibited the proliferation of cancer cell. Nevertheless, the mechanism has not been completely clarified. The purpose of the study is to explore the mechanisms of salidroside against gastric cancer. To analyze the changes of microRNA (miRNA) in gastric cancer cells under the treatment of salidroside, the miRNA expression was analyzed by using RNA-seq in cancer cells for 24 h after salidroside treatment. The differentially expressed miRNAs were clustered and their target genes were analyzed. Selected miRNA and target mRNA genes were further verified by q-PCR. The expressions of target genes in cancer cells were detected by immunohistochemistry. Cancer cell apoptotic index was significantly increased after salidroside treatment. The proliferation of gastric cancer cells were blocked at S-phase cell cycle. The expression of 44 miRNAs changed differentially after salidroside treatment in cancer cells. Bioinformatic analysis showed that there were 1384 target mRNAs corresponding to the differentially expressed miRNAs. Surprisingly, salidroside significantly up-regulated the expression of tumor suppressor miR-1343-3p, and down-regulated the expression of MAP3K6, STAT3 and MMP24-related genes. Salidroside suppressed the growth of gastric cancer by inducing the cancer cell apoptosis, arresting the cancer cell cycle and down-regulating the related signal transduction pathways. miRNAs are expressed differentially in gastric cancer cells after salidroside treatment, playing important roles in regulating proliferation and metastasis. Salidroside may suppress the growth of gastric cancer by up-regulating the expression of the tumor suppressor miR-1343-3p and down-regulating the expression of MAP3K6 and MMP24 signal molecules.

Keywords: Salidroside; gastric cancer cell; microRNA (miRNA); proliferation; signal molecules.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Proliferation
  • Glucosides*
  • Humans
  • MAP Kinase Kinase Kinases / drug effects
  • MAP Kinase Kinase Kinases / metabolism
  • Matrix Metalloproteinases, Membrane-Associated
  • MicroRNAs* / drug effects
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • Phenols*
  • Stomach Neoplasms* / drug therapy
  • Stomach Neoplasms* / genetics

Substances

  • Glucosides
  • Matrix Metalloproteinases, Membrane-Associated
  • MicroRNAs
  • MIRN-1343 microRNA, human
  • MMP24 protein, human
  • Phenols
  • rhodioloside
  • MAP kinase kinase kinase 6
  • MAP Kinase Kinase Kinases

Grants and funding

This work is supported by the National Natural Science Foundation of China [No. 81172135], Key Scientific Research Program of Xizang Autonomous Region and Xizang Minzu University [No. XZ202101ZR0074G and No.20MDT02], Graduate research and innovation projects [No. Y2024002, Y2024005], Research project of Chunhui plan of Ministry of Education of China [No. 202070310] and the Natural Science Basic Research Plan in Shaanxi Province of China [No.2020JM-590, 2022JM-465].