LINC00152 is a potential biomarker involved in the modulation of biological characteristics of residual colorectal cancer cells following chemoradiotherapy

Abstract

Concurrent radiotherapy and chemotherapy is a widely used, comprehensive treatment for rectal cancer. By studying the impact of concurrent chemoradiotherapy on the invasion and migration of colorectal cancer (CRC) cells and researching the associated molecular mechanisms, the present study aimed to provide a novel method to improve the therapeutic effect of this treatment against CRC. Human HCT116 and HT29 CRC cells were simultaneously treated with 4 Gy of 6 MV X-rays and 10 µmol/l 5-fluorouracil to establish a residual cell model. Transwell migration and invasion experiments were used to analyse the invasion and migration of the cells. The expression of long non-coding (lnc)RNAs was detected using a gene chip, and reverse transcription-quantitative polymerase chain reaction analysis was used to determine lncRNA expression levels. Specific small interfering RNAs were transfected into HCT116 residual cells to silence the expression of the identified key genes. The migration and invasion of residual CRC cells were demonstrated to be significantly increased compared with the original cells. Pvt1 oncogene, long-chain non-protein-coding RNA 152 (LINC00152), and MIR22 host gene were selected as potential targets. However, the migration and invasion of residual HCT116 cancer cells were only significantly decreased following silencing of LINC00152 expression. LINC00152 may therefore be a potential biomarker involved in modulation of the biological characteristics of residual CRC cells following chemoradiotherapy.

Higher Expression of Linc00152 Promotes Bladder Cancer Proliferation and Metastasis by Activating the Wnt/β-Catenin Signaling Pathway

“…Linc00152 has been reported to be involved in multiple physiological and pathological processers such as colorectal cancer, gallbladder cancer, and breast cancer [11,12,22]. Recent studies have revealed that high expression of Linc00152 promotes cell proliferation, migration, and invasion [11,12,22]. However, the detailed role of Linc00152 and its related mechanisms involved in BC remain unclear.…”

“…lncRNA- Linc00152 is an intergenic lncRNA mapped to 2p11.2, and previous studies have revealed its function as an oncogene in gastrointestinal cancer, clear cell renal cell carcinoma, hepatocellular carcinoma, and gallbladder carcinoma [9–12]. Linc00152 can also cause cancer cell proliferation and growth via the epidermal growth factor receptor (EGFR)/mammalian target of rapamycin (mTOR) signaling pathway, or promote cancer cell migration and invasion by regulating epithelial-to-mesenchymal transition (EMT) [11–14]. However, the Linc00152 expression and its related mechanism in BC has not yet been reported.…”

PVT1 Long Non-coding RNA in Gastrointestinal Cancer

“…These findings were consistent with the results obtained using cellular models of acquired drug resistance in vitro. HCT116 colon cancer cells resistant to the combination of 5-FU and radiation displayed increased levels of PVT1 compared to the parental cell line when evaluated using a human lncRNA Expression Array (158). Assessment of PVT1 transcript levels by quantitative RT-PCR in LOVO and RKO colon cancer cell lines with acquired resistance to cisplatin, or HCT8 and HCT116 with secondary resistance to 5-FU also evidenced the transcriptional upregulation of PVT1 lncRNA (70,157).…”

Biomarkers in Colorectal Cancer: Current Research and Future Prospects

“…Interestingly, not all CRC cell lines show invasive behavior attributable to PVT1 . The HCT116 CRC cell line did not show greater invasiveness compared to control lines [ 141 ]. Overall, the correlation of high PVT1 expression and reduced overall survival in CRC as well as other types of cancer has been encapsulated in a meta-analysis of 39 studies [ 142 ].…”

“…These changes could be reversed by siRNA targeting PVT1 . Furthermore, the HCT116 CRC cell line resistant to 5-FU displays high levels of PVT1 expression and upregulation of MRP1 [ 141 , 146 ]. siRNA against PVT1 led to reduced cell survival and increased apoptosis as well as reduced MRP1 expression [ 146 ].…”