Circular RNA circABCC4 as the ceRNA of miR‐1182 facilitates prostate cancer progression by promoting FOXP4 expression

Abstract

In recent years, circular RNAs (circRNAs) have been identified to be essential regulators of various human cancers. However, knowledge of the functions of circRNAs in prostate cancer remains very limited. The correlation between circABCC4 and human cancer is largely unknown. This study aims to investigate the biological functions of circABCC4 in prostate cancer progression and illustrate the underlying mechanism. We found that circABCC4 was remarkably up‐regulated in prostate cancer tissues and cell lines and promoted FOXP4 expression by sponging miR‐1182 in prostate cancer cells. CircABCC4 knockdown markedly suppressed prostate cancer cell proliferation, cell‐cycle progression, migration and invasion in vitro. Furthermore, silencing of the circRNA also delayed tumor growth in vivo. Taken together, our findings indicated that circABCC4 facilitates the malignant behaviour of prostate cancer by promoting FOXP4 expression through sponging of miR‐1182. The circABCC4–miR‐1182‐FOXP4 regulatory loop may be a promising therapeutic target for prostate cancer intervention.

Circ‐MTO1 correlates with favorable prognosis and inhibits cell proliferation, invasion as well as miR‐17‐5p expression in prostate cancer

“…Evidence correlating circRNAs with the pathogenesis of prostate cancer is preliminary but promising. For instance, circ‐ABCC4 advocates the progression of prostate cancer by acting as competing endogenous RNA (ceRNA) of miR‐1182 via promoting the expression of forkhead box P4 . Another study reveals that circ_0001206 is decreased in prostate cancer tumor tissue and represses cell proliferation, migration and invasion in prostate cancer cells .…”

“…In this study, we discovered that (a) circ-MTO1 expression was the expression of forkhead box P4. 12 Another study reveals that circ_0001206 is decreased in prostate cancer tumor tissue and represses cell proliferation, migration and invasion in prostate cancer cells. 17 Additionally, a recent research discloses that the decreased circ-itchy E3 ubiquitin-protein ligase associates with more severe pathological T stage, increased lymph node metastasis risk and worse survival in patients with prostate cancer.…”

“…In recent years, circRNAs have been revealed as genetic factors that play critical roles in various cancers, such as promoting cancer progression by regulating cancer cell functions and presenting with potential as prognostic biomarkers . Additionally, circRNAs are increasingly implicated in prostate cancer as well; however, the relevant studies are not as abundant as the studies of other cancers . Circular RNA‐mitochondrial tRNA translation optimization 1 (circ‐MTO1) is a novel circRNA that is previously reported as an anti‐tumor gene, which inhibits liver fibrosis to prevent hepatocellular carcinoma and represses progression of lung cancer and breast cancer .…”

“…[9][10][11] Additionally, circRNAs are increasingly implicated in prostate cancer as well; however, the relevant studies are not as abundant as the studies of other cancers. 12,13 Circular RNA-mitochondrial tRNA translation optimization 1 (circ-MTO1) is a novel circRNA that is previously reported as an anti-tumor gene, which inhibits liver fibrosis to prevent hepatocellular carcinoma and represses progression of lung cancer and breast cancer. 14,15 And circ-MTO1 has also been reported to express in prostate cancer (http://www.circb ase.org/), Based on these facts, we supposed that circ-MTO1 might play a crucial role in prostate cancer.…”

YY1‐induced upregulation of FOXP4‐AS1 and FOXP4 promote the proliferation of esophageal squamous cell carcinoma cells

“…Previously, FOXP4‐AS1 has been reported to be an oncogene in colorectal cancer (Li et al, 2017) and osteosarcoma (Yang et al, 2018). Cancer facilitator role of FOXP4 was researched in breast cancer (Ma and Zhang, 2019), prostate cancer (Huang et al, 2019), and renal carcinoma (Xiong et al, 2019). However, the role and molecular mechanism of FOXP4‐AS1 and FOXP4 in ESCC are still unclear.…”