Tβ4-17 peptide enhances the chemo-sensitivity of ovarian cancer cells to DDP by affecting NF-κB signaling pathway

This study investigated whether Tβ4-17, a small bioactive peptide derived from thymosin β4 and identified via iTRAQ technology, could enhance the sensitivity of cisplatin (DDP)-resistant ovarian cancer cells to chemotherapy. Using in vitro models of DDP-resistant ovarian cancer cell lines, the researchers examined the effects of Tβ4-17 alone and in combination with DDP on cell proliferation, migration, and apoptosis. Multiple assays were employed, including CCK8 viability assays, EDU fluorescence proliferation assays, cell scratch (wound healing) assays, qRT-PCR, and Western blot. The study found that Tβ4-17 combined with DDP significantly inhibited proliferation and migration of resistant cells and promoted apoptosis compared to either agent alone. Mechanistically, the researchers reported that NF-κB p65 was highly expressed in DDP-resistant cells, and that Tβ4-17 down-regulated NF-κB p65 protein expression. Use of NF-κB inhibitors and activators further supported this proposed pathway. Key limitations include the exclusive use of cell-line models with no animal or human data, the preprint status of the work, and the absence of in vivo validation. Findings are preliminary and require further study.

Why this grade: All experiments were conducted exclusively in cisplatin-resistant ovarian cancer cell lines with no animal models or human subjects, and the work has not yet completed peer review as a preprint.