Antimicrobial and antitumor properties of anuran peptide temporin-SHf induce apoptosis in A549 lung cancer cells.

Temporin-SHf is a linear, ultra-short, hydrophobic, α-helix, and phe-rich cationic antimicrobial peptide. The antitumor activities and mechanism of temporin-SHf-induced cancer cell death are unknown. The temporin-SHf was synthesized by solid-phase Fmoc chemistry and antimicrobial and antitumor activities were investigated. Temporin-SHf was microbiocidal, non-hemolytic, and cytotoxic to human cancer cells but not to non-tumorigenic cells. It affected the cancer cells' lysosomal integrity and caused cell membrane damage. The temporin-SHf inhibited A549 cancer cell proliferation and migration. It is anti-angiogenic and causes cancer cell death through apoptosis. The molecular mechanism of action of temporin-SHf confirmed that it kills cancer cells by triggering caspase-dependent apoptosis through an intrinsic mitochondrial pathway. Owing to its short length and broad spectrum of antitumor activity, temporin-SHf is a promising candidate for developing a new class of anticancer drugs.

Antitumor activity of Tigerinin-1: Necroptosis mediates toxicity in A549 cells.

BACKGROUND: Tigerinins are antimicrobial peptides (AMPs) derived from the skin secretions of the Indian bullfrog Hoplobatrachus tigerinus. METHODS: Tigerinin-1 (FCTMIPIPRCY-Am) peptide was synthesized by solid-phase Fmoc chemistry and investigated its antitumor activities. RESULTS: Tigerinin-1 was cytotoxic to human cancer cells. It causes necrosis by damaging the cell membrane and loss of lysosome integrity. Tigerinin-1triggers the expression of necroptosis pathway proteins. It generates reactive oxygen species (ROS) and induces oxidative stress-mediated genotoxicity. Tigerinin-1 inhibits cancer cell proliferation, reduces neovascularization, and down-regulates the vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2), and fibroblast growth factor (FGF) genes. CONCLUSIONS: Tigerinin-1 exhibited its potent antitumor properties in this study. GENERAL SIGNIFICANCE: Tigerinin-1 can be beneficial for developing novel therapeutics for cancer.

Hyperthermia enhances methyl methanesulfonate-induced adaptive response in meiotic cells of grasshopper Poecilocerus pictus.

To understand the role of hyperthermia (HT) in adaptive response, methyl methanesulfonate (MMS) adapted meiotic cells of Poecilocerus pictus were used. Poecilocerus pictus were treated with conditioning (L) or challenging (H) dose of MMS and 2-h time lag (TL) between these doses (L-2h-H) (combined) was employed. Different treatment schedules were used to analyse the influence of HT on MMS-induced adaptive response namely pre; inter; post-treatment and cross-adaptation. After each treatment schedules, chromosomal anomalies were analysed. The frequencies of chromosomal anomalies induced by conditioning and challenging doses of MMS were significantly higher (P < 0.0001) compared to that of the control or HT groups. The combined treatments resulted in significant reduction of chromosomal anomalies compared to additive effect of MMS (P < 0.0001). The pre, inter, post and cross-adaptation treatments with HT reduced the frequencies of chromosomal anomalies compared to the challenge and combined treatments with MMS. There is a protection against MMS-induced chromosomal anomalies by HT in in vivo P.pictus. This is the first report to demonstrate that HT enhances the MMS-induced adaptive response in in vivo meiotic cells.