In this review, I plan to place a special emphasis on HA/CD44-induced signaling pathways and the presence of several novel miRNAs (e.g., miR-10b/miR-302/miR-21) and lncRNAs (e.g., UCA1) together with their target functions (e.g., tumor cell migration, invasion, and chemoresistance) during cancer development and progression.
Upregulated lncRNA-UCA1 contributes to metastasis of bile duct carcinoma through regulation of miR-122/<i>CLIC1</i> and activation of the ERK/MAPK signaling pathway.
Long noncoding RNA UCA1 promotes osteosarcoma metastasis through CREB1-mediated epithelial-mesenchymal transition and activating PI3K/AKT/mTOR pathway.
Gastric cancer (GC) has a clear predilection for metastasis toward omentum which is primarily composed of adipose tissue, combine with our previous research that long non-coding RNA Urothelial cancer associated 1 (UCA1) could promote the peritoneal metastasis of GC, we put forward the hypothesis that fatty acids (FAs) might contribute to these phenomena and a connection between FAs and UCA1 might exist.
The UCA1-miR-204-CXCR4 regulatory network regulated the growth and metastasis of PCa, providing new insight in the management of patients with such malignancy.
Here, we found that the long noncoding RNA urothelial carcinoma-associated 1 (UCA1) was highly expressed in ACC tissues and closely associated with the TNM stage and metastasis of ACC patients.
Long noncoding RNA urothelial carcinoma associated 1 (UCA1) has been implicated in the growth and metastasis of colorectal cancer (CRC), and autophagy contributes to tumorigenesis and cancer cell survival.
An increasing number of studies indicated that dysregulation of human urothelial carcinoma associated 1 (UCA1) is associated with progression of tumor and metastasis in various cancers including CRC.
This study thus reveals a new mechanism by which a hypoxic microenvironment promotes tumor metastasis, and highlights UCA1 as a potential biomarker for predicting the metastasis of gastric cancer to guide clinical treatment.
In the present study, we found that UCA1 was aberrantly upregulated in gastric cancer tissues and gastric cancer cell lines, and was associated with TNM stage and metastasis.
Taken together, UCA1 might promote proliferation and migration of glioma, to regulate the tumor growth and metastasis via miR-182 dependent iASPP regulation.
Accumulating evidences indicated that UCA1 expression was up-regulated in various cancers, and high UCA1 expression was correlated with metastasis and prognosis.
In the present work, we revealed that UCA1 silencing suppressed proliferation and metastasis and induced apoptosis of OSCC cell lines in vitro and in vivo, which might be related to the activation level of the WNT/β-catenin signaling pathway.
Our findings provide the convincing evidence that the UCA1 plays an important role in the metastasis of EC and may serve as a novel molecular marker to predict the aggressive tumor progression and unfavorable prognosis of EC patients.