Abstract
Lactoferricin peptide (LP) has been reported to control cancer cell proliferation. NF-κB interacting lncRNA (NKILA) is a tumor suppressor in several cancers. We aimed to explore the potential function of the truncated LP (TLP) in the prevention of cervical cancer cell proliferation. Bioinformatics analysis via PPA-Pred2 showed that 18-aa N-terminus of truncated lactoferricin peptide (TLP18, FKCRRWQWRMKKLGAPSI) shows higher affinity with nuclear factor kappaB (NF-κB) than LP. The effects of LP and TLP18 on cervical cancer cells SiHa and HeLa and the related mechanisms were explored by investigating NF-κB and lncRNA-NKILA. TLP18 shows an inhibitory rate up to 0.4-fold higher than LP on the growth of cervical cancer cells (P<0.05). NKILA siRNA promoted cell growth whether LP or TLP18 treatment (P<0.05). TLP18 treatment increases the level of lncRNA-NKILA and reduces the level of NF-κB up to 0.2-fold and 0.6-fold higher than LP (P<0.05), respectively. NKILA siRNA increased the levels of NF-κB, cleaved caspase-3, and BAX (P<0.05). TLP18 increased apoptotic cell rate up to 0.2-fold higher than LP, while NKILA siRNA inhibited cell apoptosis cell growth even LP or TLP18 treatment. Truncated Lactoferricin peptide controls cervical cancer cell proliferation via lncRNA- NKILA/NF-κB feedback loop.
Published Version
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