GAS5 expression was markedly decreased in GC tissues and cell lines, and its low expression was strongly related to GC metastasis and unsatisfactory prognosis.
Functionally, GAS5 is involved in cell proliferation, metastasis, invasion, apoptosis, epithelial-mesenchymal transition (EMT), and drug resistance, among others, via multiple molecular mechanisms, such as binding to DNA sequences, forming RNA-DNA triplex complex, triggering or suppressing the expression of genes, binding proteins to form chromatin-modifying complex, which activates or represses gene expression, and acting as miRNA sponge to suppress miRNA expression, leading to regulation of miRNA target genes.
Thus, our data suggested that lncRNA GAS5 could effectively sponge miR-222 to modulate human B lymphocytic leukaemia cell tumourigenesis and metastasis.
The expression of lncRNA-GAS5 and lncRNA-FAL1 revealed a significant association with tumor node metastasis staging (P < 0.042 and P < 0.001, respectively).
Analysis of clinical samples from MM patients showed that the rate of reduced GAS5 expression, relative to that in adjacent noncancerous tissues, was significantly lower for tumors from patients with advanced disease (76.6%, P < 0.001), as evidenced by larger tumor size, higher TNM stage, and higher incidences of ulceration and metastasis (P < 0.001 for all).
Overexpression of GAS5 inhibited proliferation, cell cycle progression, invasion, migration while inducing apoptosis of cervical cancer cells as well as suppressed tumor growth and metastasis in nude mice.
Mechanistically, GAS5 functioned as a tumor suppressor in HCC metastasis through directly interacting with miR-182 and abrogating its oncogenic function in this setting.
In this study, we investigated the effect of long noncoding RNA (lncRNA) GAS5 on the angiogenesis, invasion, and metastasis of CRC, and the involvement of the Wnt/β-catenin signaling pathway.
Additionally, GAS5 promoted gemcitabine-induced tumor growth and metastasis inhibition, as determined by Ki-67 staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), bioluminescence imaging, and the detection of cell-like properties and EMT in vivo.
Accumulating evidence demonstrates that the long non-coding RNA Growth Arrest-Specific 5 (Gas5) has practical significance in cancer progression and metastasis.
While the LncRNA GAS5 expression in tissues, plasma and exosomes were associated with the tumor node metastasis (TNM) stage, Dukes stage, lymph node metastasis (LNM), local recurrence rate and distant metastasis rate, the MiR-221 expression in tissues, plasma and exosomes were associated with tumor size, TNM stage, Dukes stage, LNM, local recurrence rate and distant metastasis rate.
The precise role of GAS5 in pancreatic cancer (PC) progression is currently unknown, so the aim of this study was to explore the functional participation of GAS5 in PC metastasis.
This meta-analysis suggests GAS5 lncRNA may be a useful diagnostic and prognostic cancer biomarker, and may be especially useful for identifying patients prone to developing lymph node or distant metastasis.
In current two-stage, case-control study, we systematically evaluated the potential role of lncRNA GAS5 and its genetic variation rs145204276 in the development and metastasis process of CRC in a Chinese population.
The data show that no significant differences of GAS5 expression were observed between normal ovarian epithelium and benign epithelial lesions; however, GAS5 expression was lower in EOC tissues compared with normal ovarian epithelial tissues (6.44-fold), which was closely related to lymph node metastasis (P=0.025) and tumor node metastasis stage (P=0.035).