Second Department of General Surgery, Shanxi Provincial Cancer Hospital, TaiYuan 030013, Shanxi, China.
Department of Endocrinology, Shanxi Bethune Hospital, TaiYuan 030032, Shanxi, China.
Immunobiology. 2022 Nov;227(6):152295. doi: 10.1016/j.imbio.2022.152295. Epub 2022 Oct 26.
Previous works have outlined the pivotal involvement of long intergenic non-coding RNA (lincRNA) in cancer progression, while the efficiency of LINC01234 in pancreatic cancer remained obscure. The purpose of this research is to unravel the regulatory mechanism of LINC01234 in pancreatic cancer via modulating microRNA (miR)-513a-3p and hexose 6-phosphate dehydrogenase (H6PD).
Pancreatic cancer cells were cultured and clinical tissue specimens were collected. LINC01234, miR-513a-3p and H6PD levels in pancreatic cancer cells and tissues were examined. Plasmids altering LINC01234, miR-513a-3p and H6PD expression were transfected into pancreatic cancer cells to assess the change in biological behaviors of pancreatic cancer cells. The targeting relations among LINC01234, miR-513a-3p and H6PD were validated.
LINC01234 and H6PD levels were elevated while miR-513a-3p level was reduced in pancreatic cancer cells and tissues. LINC01234 deficiency hindered the malignant biological activities of pancreatic cancer cells. MiR-513a-3p depletion or H6PD elevation could abrogate the inhibitory effects of LINC01234 silencing on pancreatic cancer cells. LINC01234 sponged miR-513a-3p that targeted H6PD.
The reduced LINC01234 exerts inhibitory impacts on pancreatic cancer cells via targeting miR-513a-3p to restrain H6PD level. The current study broadens the understanding of LINC01234 function and affords novel therapeutic targets for pancreatic cancer treatment.
先前的研究已经概述了长链非编码 RNA（lncRNA）在癌症进展中的关键作用，而 LINC01234 在胰腺癌中的作用尚不清楚。本研究旨在通过调节 microRNA（miR）-513a-3p 和己糖 6-磷酸脱氢酶（H6PD）来揭示 LINC01234 在胰腺癌中的调控机制。
培养胰腺癌细胞并收集临床组织标本。检测胰腺癌细胞和组织中 LINC01234、miR-513a-3p 和 H6PD 的水平。转染改变 LINC01234、miR-513a-3p 和 H6PD 表达的质粒，评估胰腺癌细胞生物学行为的变化。验证 LINC01234、miR-513a-3p 和 H6PD 之间的靶向关系。
LINC01234 和 H6PD 的水平在胰腺癌细胞和组织中升高，而 miR-513a-3p 的水平降低。LINC01234 缺失抑制了胰腺癌细胞的恶性生物学活性。miR-513a-3p 耗竭或 H6PD 升高可消除 LINC01234 沉默对胰腺癌细胞的抑制作用。LINC01234 吸附 miR-513a-3p 靶向 H6PD。
减少的 LINC01234 通过靶向 miR-513a-3p 抑制 H6PD 水平对胰腺癌细胞发挥抑制作用。本研究拓宽了对 LINC01234 功能的认识，为胰腺癌的治疗提供了新的治疗靶点。
