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LncRNA GUSBP11 regulates malignant biological behaviors of gastric cancer cells through the miR-339-5p/MDM2 axis
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Abstract:
[Abstract] Objective: To investigate the effect of long non-coding RNA glucuronidase β pseudogene 11 (GUSBP11) regulating miR-339-5p/mouse two-minute homolog 2 (MDM2) axis on the proliferation, migration, and invasion of gastric cancer AGS cells. Methods: Cancerous and adjacent tissues from 25 gastric cancer patients who underwent surgical treatment at Foshan Hospital of Traditional Chinese Medicine Affiliated to Guangzhou University of Chinese Medicine from December 2023 to June 2024 were collected. Gastric cancer AGS cells and normal gastric mucosal epithelial GES-1 cells were routinely cultured. The control plasmids and knockdown plasmids were transfected into AGS cells using transfection reagents, dividing the cells into Ctrl group, sh-NC group, sh-GUSBP11 group, sh-GUSBP11 + anti-NC group, and sh-GUSBP11 + anti-miR-339-5p group. The mRNA expression of GUSBP11, miR-339-5p, and MDM2 in gastric cancer tissues and cells of each group was detected by qPCR. A dual-luciferase reporter gene assay was used to detect the targeting relationship between GUSBP11 or MDM2 and miR-339-5p. EdU staining, scratch healing assay, and Transwell chamber assay were adopted to assess the proliferation, migration, and invasion abilities of AGS cells, respectively. WB assay was used to measure the protein expression of CDK1, MMP-2, and MMP-9 in AGC cells. The effects of GUSBP11 knockdown on tumor growth were examined through AGS cell xenograft experiments. Results: The mRNA expression of GUSBP11 and MDM2 were significantly upregulated in gastric cancer tissues and cells (both P < 0.05), while miR-339-5p was significantly downregulated (P < 0.05). A targeting relationship was found between GUSBP11 and miR-339-5p, as well as between MDM2 and miR-339-5p. Knockdown of GUSBP11 in AGS cells significantly inhibited MDM2 protein expression and promoted miR-339-5p expression, while inhibition of miR-339-5p promoted MDM2 protein expression. GUSBP11 knockdown significantly inhibited the proliferation, migration, and invasion of AGS cells, while inhibition of miR-339-5p reversed this effect. GUSBP11 knockdown significantly inhibited the protein expression of CDK1, MMP-2, and MMP-9, and inhibition of miR-339-5p reversed this effect. Furthermore, GUSBP11 knockdown significantly inhibited the growth of AGS cell xenografts. Conclusion: GUSBP11 is highly expressed in gastric cancer tissues and cells, and knocking down GUSBP11 expression may inhibit malignant biological behaviors of gastric cancer cells through regulating the miR-339-5p/DM2 axis.
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