Long non-coding RNA AB019562 promotes cell proliferation and metastasis in human hepatocellular carcinoma

Abstract

Increasing evidence has supported the prognostic and therapeutic values of long non-coding RNAs (LncRNAs) in human tumorigenesis. Hepatocellular carcinoma (HCC), as one of the most refractory diseases, continues to warrant investigation for novel clues to enable early diagnosis. In the present study, the role of LncRNA AB019562 in cell proliferation and metastasis was investigated in HCC. Reverse transcription-quantitative polymerase chain reaction analysis was performed to determine the expression of AB019562 in clinical HCC samples and cultured HCC cells. In addition, a specific small interfering RNA against AB019562 was designed and transfected into HCC cells. A3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and a transwell assay were used to assess the effects of AB019562 knockdown on cell proliferation and metastasis, respectively. The results revealed that the expression of AB019562 was increased 4-fold in the clinical HCC tissues, compared with adjacent non-cancerous tissue counterparts. AB019562 was differentially expressed in the HCC cell lines. The knockdown of AB019562 reduced the rate of cell proliferation by 28.6% in HepG2 cells and by 24% in SMMC-7721 cells. Cell cycle assays revealed that the proportion of cells in the G0/G1 phase was significantly increased, whereas those in the S and G2/M phases were decreased in the AB019562-knockdowncells. The results of the transwell assay showed that the knockdown of AB019562 inhibited cell migration abilities by up to 67% in the HepG2 cells and 63% in the SMMC-7721 cells, and significantly suppressed invasive abilities by up to 75% in the HepG2 cells and 60% in the SMMC-7721 cells. Furthermore, AB019562 knockdown increased the apoptotic rates of the two cell lines and activated the expression of caspase-3, but not caspase-8. These data demonstrated the pro-oncogenic properties of AB019562 and suggested that AB019562 may serve as a novel biomarker for the diagnosis and treatment of patients with HCC.

Long Noncoding RNA MIR100HG Knockdown Attenuates Hepatocellular Carcinoma Progression by Regulating MicroRNA-146b-5p/Chromobox 6

“…The lncRNA elevation often facilitates HCC progression [ 25 ]. The expression of lncRNAs, such as MALAT1 [ 10 ], AB019562 [ 24 ], and CARLo-5 [ 26 ], is enhanced in HCC patients. In the present research, MIR100HG expression was elevated in HCC, indicating that MIR100HG may be an oncogenic lncRNA in HCC.…”

“…qRT-PCR and western blot were performed as previously described [ 24 ]. The primers are depicted in Table 1 .…”

“…Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western Blot. qRT-PCR and western blot were performed as previously described [24]. The primers are depicted in Table 1.…”

Behind the curtain of non-coding RNAs; long non-coding RNAs regulating hepatocarcinogenesis

“…TINCR lncRNA is found to be upregulated in HCC cells acting as an oncogene regulating differentiation, invasion and metastasis of tumor cells[ 61 ]. AB019562 is reported to be upregulated in HCC cells; its knockdown inhibits cell proliferation, arrests cell cycle at G0/G1 phase, suppresses cellular metastasis, induces apoptosis and activates caspase-3 activity[ 62 ]. LncARSR is a long non-coding RNA that regulates the sensitivity of the tumor cells to doxorubicin.…”

Silencing long intergenic non‑coding RNA 00707 enhances cisplatin sensitivity in cisplatin‑resistant non‑small‑cell lung cancer cells by sponging miR‑145

“…Long non-coding RNAs (lncRNAs) are non-protein coding RNAs that are greater than 200 nucleotides in length (3). Numerous studies have indicated that lncRNAs are capable of regulating gene expression at the transcriptional, post-transcriptional and epigenetic levels, and serve an important role in human cancer development, prognosis and drug resistance (4,5). Recent studies have associated certain lncRNAs, including CCAT1 (6) and TRPM2-AS (7), with DDP resistance in lung cancer.…”