Effects of sesamin on the chemosensitivity, invasiveness and immune evasion mechanism of human lung adenocarcinoma

Lung adenocarcinoma (LUAD) is a major cause of cancer-related mortality worldwide. Sesamin is a lignan with potent anticancer properties and promising therapeutic potential. In the present study, it was aimed to investigate the specific mechanisms through which sesamin reduces cell invasiveness and cancer-associated immunosuppression in LUAD cells. The effects of sesamin on LUAD cell invasiveness were investigated using a wound healing assay and anoikis resistance assay. NK-92 MI cells were used to analyze cancer-associated immunosuppression upon sesamin treatment. The therapeutic effect of sesamin in LUAD was measured using a subcutaneous mouse model. Our results indicated that sesamin inhibited the proliferation, survival and migration of LUAD cells (A549 and CL1-5) in a dose-dependent manner. Sesamin also enhanced the proapoptotic effects of chemotherapeutic agents such as docetaxel and paclitaxel through the activation of the caspase-3/poly(ADP-ribose) polymerase pathway. In addition, sesamin reduced cancer cell migration and anoikis resistance by downregulating the expression of N-cadherin and inhibiting the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. It also induced the downregulation of programmed death ligand 1 through hsa-microRNA-34a-5p, resulting in the increased cytotoxicity of natural killer cells. This sequence of events consequently interfered with the immune evasion mechanism of LUAD cells. In conclusion, sesamin has a multifaceted effect on the migration, anoikis resistance and antitumor immunity of LUAD cells, indicating its potential as adjunctive therapy.

• Publication year

  2025

• Venue

  International Journal of Molecular Medicine

• Publication date

  2025-09-11

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.3892/ijmm.2025.5635PMID 40937589PMCID 12440275
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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