Journal
NEOPLASMA
Volume 69, Issue 5, Pages 1138-+Publisher
AEPRESS SRO
DOI: 10.4149/neo_2022_220111N42
Keywords
colorectal cancer; PSMB8-AS1; miR-1299; ADAMTS5
Categories
Funding
- Open Proj- ect in 2018 of the National Clinical Research Center for Geriatric Disorders
- [NCRCG-PLAGH-2018002]
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This study found that PSMB8-AS1 is significantly upregulated in CRC, and downregulation of PSMB8-AS1 can inhibit the malignant growth behaviors of CRC cells. PSMB8-AS1 regulates ADAMTS5 by sponging miR-1299, promoting the growth of CRC cells.
Long non-coding RNAs (lncRNAs) have been reported to be vital participants in tumor progression. Recently, lncRNA PSMB8-AS1 has been uncovered to facilitate pancreatic cancer progression by regulating miR-382-3p/STAT1/PD-L1 network. Nonetheless, the role of PSMB8-AS1 and its underlying mechanism have not been well-explored in colorectal cancer (CRC). The expression of RNAs or proteins was detected via qRT-PCR or western blot assays. Functional assays were involved in evaluating the effects of PSMB8-AS1/miR-1299/ADAMTS5 on the malignant behaviors of CRC cells. The molecular mechanism of PSMB8-AS1 was explored via mechanism analyses in CRC cells. Based on experimental results, PSMB8-AS1 expression was notably higher in CRC cell lines than in normal cells. The downregulation of PSMB8-AS1 repressed cell viability, proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of CRC while promoting cell apoptosis. It was also revealed that PSMB8-AS1 could sponge miR-1299 to upregulate ADAMTS5 in CRC cells. In rescue assays, we further discovered that miR-1299 inhibition or ADAMTS5 overexpression abrogated the suppres-sive influence of PSMB8-AS1 deficiency on CRC cell growth. In addition, PSMB8-AS1 was validated to induce M2 polariza-tion. In conclusion, PSMB8-AS1 sponges miR-1299 to increase PSMB8-AS1 expression, thus promoting CRC cell growth.
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