Purpose: To elucidate the potential role of long non-coding RNA (lncRNA) DUXAP8 in the malignant progression of colorectal cancer (CRC) and its possible molecular mechanism.
Methods: The expression level of lncRNA DUXAP8 in CRC tissues and matched paracancerous tissues was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, its level in CRC patients with different tumor sizes and tumor grades was determined. The regulatory effects of DUXAP8 on the behaviors of CRC cells were evaluated by cell counting kit-8 (CCK-8), 5-Ethynyl-2'- deoxyuridine (EdU) and Transwell assay. The interaction between LSD1, EZH2 and DUXAP8 was evaluated by RNA-protein interactions and RIP assay. Linear regression analyses were conducted to examine the correlation between DUXAP8 and LSD1, EZH2.
Results: LncRNA DUXAP8 was upregulated in CRC tissues and cell lines. Its level remained higher in CRC with larger tumor size or higher tumor grade. Knockdown of DUXAP8 suppressed the proliferative, migratory and invasive abilities of DLD-1 and SW480 cells. Both RF classifier and SVM classifier predicted the pronounced accuracies of LSD1 and EZH2. RIP assay further demonstrated the interaction between DUXAP8 and LSD1, EZH2. Knockdown of LSD1 or EZH2 could attenuate the proliferative rate of CRC cells. Moreover, the mRNA levels of LSD1 and EZH2 were positively correlated with DUXAP8 in CRC.
Conclusions: LncRNA DUXAP8 accelerates the malignant progression of CRC via positively regulating EZH2 and LSD1.
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Pathol Res Pract
December 2024
Research Fellow School of Life Sciences, University of Sussex, Brighton, UK. Electronic address:
Humans have more than 270,000 lncRNAs. Among these, lncRNA HOXA-AS2 is considered a transformative gene involved in various cellular processes, including cell proliferation, apoptosis, migration, and invasion. Thus, it can be regarded as a potential tumor marker for both diagnosis and prognosis.
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Division of Pediatric Oncology, Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
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State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
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Department of Urology, the First Affiliated Hospital of Ningbo University, 52, Liuting Street, Haishu District,Ningbo, Zhejiang 315010, China.
Neuroendocrine prostate cancer (NEPC) is a highly aggressive variant of castration-resistant prostate cancer. It is characterized by low or no expression of the androgen receptor (AR), activation of AR-independent signaling, and increased neuroendocrine phenotype. Most of NEPC is induced by treatment of androgen deprivation therapy and androgen receptor pathway inhibitors (ARPIs).
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