Abstract
Hypoxia plays a key role in colorectal cancer (CRC) metastasis, but its underlying mechanism remains largely unknown. Dicer1, an RNase, has been considered as a tumor regulator in many tumors. However, whether Dicer1 affects CRC progression under hypoxia remains uncertain. In this study, we found that Dicer1 expression was induced by hypoxia in CRC cells and it mediates hypoxia-induced CRC cell progression. Furthermore, we found that the expression of tRF-20-MEJB5Y13, a small non-coding RNA derived from tRNA, was increased under hypoxic conditions, and its upregulation by Dicer1 resulted in hypoxia-induced CRC cell invasion and migration. These results advance the current understanding of the role of Dicer1 in regulating hypoxia signals and provide a new pathway for the development of therapeutic interventions for inhibiting cancer progression.
Highlights
Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide, which poses serious threats to public health, and its morbidity and mortality rates are increasing annually
Whether Dicer plays a functional role in the mechanism of CRC progression under hypoxic conditions and whether they are associated with tRNA-derived fragments (tRFs) remains to be elucidated
Our results were consistent with the results reported for prostate adenocarcinoma, which suggested that Dicer1 expression was upregulated and affected tumor invasion characteristics (Chiosea et al, 2006)
Summary
Colorectal cancer (CRC) is one of the most common causes of cancer-related deaths worldwide, which poses serious threats to public health, and its morbidity and mortality rates are increasing annually. Many clinical CRCs show micrometastasis of the tumor before surgery, which in itself is a complex and continuous process regulated by multiple factors and steps (Crotti et al, 2017). As the tumor cells continue to proliferate and the tumor volume increases, high demand for oxygen is created and this oxygen demand of the cells cannot be satisfied by the blood supply, which limits the use of oxygen by the cells, thereby resulting in hypoxic conditions for tumor cells (Catalano et al, 2013; Sormendi and Wielockx, 2018). Oxidative stress, and acidosis in the tumor microenvironment trigger extracellular
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