CCAT1 (Colon Cancer Associated Transcript 1)

Our findings suggest that these selected lncRNA-related SNPs may contribute to colorectal cancer risk in a sex- and site-specific manner. These preliminary results warrant further validation in larger, independent cohorts and functional studies.

Collectively, our findings delineate a novel pro-inflammatory pathway where LncRNA CCAT1 promotes macrophage inflammation by sponging miR-296-3p, thereby derepressing its target FOSL1. Therefore, targeting LncRNA CCAT1 represents a promising therapeutic strategy for treating atherosclerotic cardiovascular disease.

Importantly, in ovarian cancer cells overexpressing CCAT1, only the cpG+ modified FIT-PNA produced a bright fluorescent signal, confirmed by FACS and confocal microscopy. Our results demonstrate that strategic chemical modifications of the neighboring G base in FIT-PNA significantly enhance their brightness and specificity for RNA detection in biological systems.

The CCAT1-70aa peptide is overexpressed in HCC and linked to aggressive tumor characteristics. It promotes proliferation and invasion via the MAPK/ERK pathway, providing insights for HCC diagnosis and treatment strategies.

Given the biological functions of the dysregulated lncRNAs in NK cells from breast cancer patients, this has the potential to significantly impact the antitumor functionality of NK cells, possibly contributing to the impaired immune surveillance and tumor control commonly observed in breast cancer patients. Understanding the dysregulation of lncRNAs in NK cells may provide critical insights into the mechanisms underlying impaired NK cell function in breast cancer, offering promising approaches for developing immunotherapies aiming at restoring NK cell activity in cancer patients.

Conclusion Preoperative plasma OIP5 and CCAT1 expression are associated with radiotherapy resistance. Their role as a biomarker needs further evaluation.

Si-CCAT1 increased the levels miR-181a and decreased CPEB2 in A549 cells. In conclusion, our study has provided strong evidence that lncRNA CCAT1 decreased the sensitivity to doxorubicin in lung cancer cells by regulating the miR-181a/CPEB2 axis.

Also, lncRNA XIST revealed a sensitivity of 62% and a specificity of 61% with a cutoff point 2.4, with an AUC=65%. Our findings indicated the potential of plasma-derived exosomal lncRNA CCAT1 as a non-invasive clinical indicator for the diagnosis of CRC patients.

Additionally, the expression of PI3K/AKT/mTOR signaling pathway proteins was higher in resistant cells compared to their sensitive counterparts, and silencing CCAT1 in AGS/DDP cells resulted in reduced expression of these proteins. In conclusion, the above studies demonstrated that LncRNA CCAT1 induced cisplatin resistance in gastric cancer cells.

The functional suppression of CCAT1 holds promise in enhancing the sensitivity to erlotinib by reversing EMT through the miR-181a-5p/ROCK2 signaling pathway. These findings provide valuable insights into the mechanisms underlying erlotinib resistance in CCA and the potential strategies for its treatment.

At larger distances from the gene, the CCAT1 transcripts appeared spliced, implying that most CCAT1 transcripts undergo post-transcriptional splicing in the zone of the active gene. Finally, we show that unspliced CCAT1 transcripts can be detected in the cytoplasm during splicing inhibition, which suggests that there are several CCAT1 variants, spliced and unspliced, that the cell can recognize as suitable for export.