截短型乳铁蛋白肽通过 lncRNA-NKILA/NF-κB 反馈环控制宫颈癌细胞增殖。
Truncated Lactoferricin Peptide Controls Cervical Cancer Cell Proliferation via lncRNA-NKILA/NF-κB Feedback Loop.
机构信息
Reproductive Medical Center, The First Hospital of Jilin University, Changchun 130021, China.
Department of Gynecological Oncology and Reproductive Medical Center, The First Hospital of Jilin University, Changchun 130021, China.
出版信息
Protein Pept Lett. 2022;29(3):268-280. doi: 10.2174/0929866528666211206144110.
BACKGROUND
Lactoferricin peptide (LP) has been reported to control cancer cell proliferation. NF-κB interacting lncRNA (NKILA) is a tumor suppressor in several cancers.
OBJECTIVE
We aimed to explore the potential function of the truncated LP (TLP) in the prevention of cervical cancer cell proliferation.
METHODS
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.
RESULTS
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.
CONCLUSION
Truncated Lactoferricin peptide controls cervical cancer cell proliferation via lncRNA- NKILA/NF-κB feedback loop.
背景
乳铁蛋白衍生肽（LP）已被报道可控制癌细胞增殖。核因子κB 相互作用的长非编码 RNA（NKILA）是几种癌症中的肿瘤抑制因子。
目的
本研究旨在探讨截短的 LP（TLP）在预防宫颈癌细胞增殖中的潜在作用。
方法
通过 PPA-Pred2 进行生物信息学分析表明，截短的乳铁蛋白肽（TLP18，FKCRRWQWRMKKLGAPSI）的 18 个氨基酸 N 端与核因子 kappaB（NF-κB）的亲和力高于 LP。通过研究 NF-κB 和 lncRNA-NKILA，探讨了 LP 和 TLP18 对宫颈癌 SiHa 和 HeLa 细胞的影响及其相关机制。
结果
与 LP 相比，TLP18 对宫颈癌细胞生长的抑制率高达 0.4 倍（P<0.05）。无论 LP 或 TLP18 处理，NKILA siRNA 均促进细胞生长（P<0.05）。TLP18 处理可增加 lncRNA-NKILA 的水平，并将 NF-κB 的水平降低至 0.2 倍和 0.6 倍，分别高于 LP（P<0.05）。NKILA siRNA 增加了 NF-κB、裂解的 caspase-3 和 BAX 的水平（P<0.05）。与 LP 相比，TLP18 可将凋亡细胞比率提高 0.2 倍，而 NKILA siRNA 抑制细胞凋亡，即使在 LP 或 TLP18 处理时也是如此。
结论
截短的乳铁蛋白肽通过 lncRNA-NKILA/NF-κB 反馈环控制宫颈癌细胞增殖。
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