Abstract
Here, we investigated the clinicopathological and prognostic potential of the long noncoding RNA Colon Cancer-Associated Transcript 2 (CCAT2) in human colorectal cancer (CRC). We used qPCR to quantify CCAT2 levels in 44 pairs of CRC tissues and adjacent nontumor and healthy colon mucosa tissues, and in several CRC cell lines (SW620, SW480, HT-29, LOVO, HCT116 and DLD-1) and normal human colorectal epithelial cells (HFC). We assessed the effects of CCAT2 overexpression or knockdown on the proliferation, migration and invasion by SW620 and LOVO cells using CCK-8, transwell, and wound−healing assays, respectively. We also investigated the potential interaction between CCAT2 and TAF15 through RNA pull down and rescue experiments. Lastly, we evaluated the expression of the cell cycle progression markers and GSK3β signaling pathway proteins using Western blotting. Our results showed that CCAT2 was upregulated in CRC tissues and cell lines as com-pared to controls. Ectopic expression of CCAT2 promoted CRC cell proliferation, migration and invasion, likely through direct interaction with TAF15, transcriptional activation of RAB14, and activation of the AKT/GSK3β signaling pathway. In vivo, CCAT2 promoted CRC cell growth and metastasis in nude mice. Taken together, these results highlight the actions of CCAT2 as a CRC oncogene.
Highlights
Colorectal cancer (CRC) is the third most common malignancy worldwide affecting more than 1.2 million people every year and is the fourth leading cause of cancer-associated mortality, causing more than 600,000 yearly deaths [1]
In order to assess Cancer-Associated Transcript 2 (CCAT2) expression, we first examined the levels of CCAT2 in 44 paired colorectal cancer (CRC) and adjacent normal tissues via Quantitative PCR (qPCR)
Our results revealed that CCAT2 was upregulated in CRC tissues (Figures 1A, B)
Summary
Colorectal cancer (CRC) is the third most common malignancy worldwide affecting more than 1.2 million people every year and is the fourth leading cause of cancer-associated mortality, causing more than 600,000 yearly deaths [1]. CRC incidence is higher among men than among women and strongly increases with age [2]. CRC has both hereditary and environmental causes that contribute to the gradual development of the disease through the adenoma-carcinoma sequence. CRC therapies include surgery, adjuvant radiotherapy, adjuvant chemotherapy, fluorouracil-based chemotherapy, and oxaliplatin adjuvant treatment, among others, which are applied depending on the pathological stage of each patient [3, 4]. Some patients develop radioresistance resulting in poor prognosis, which could be alleviated by early detection [5]
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