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In recent years, long non-coding RNAs (lncRNAs) have emerged for regulating the development, as well as progression in colorectal cancer (CRC), which assists in finding new targets for CRC treatment. A previous study indicated that INHBA-AS1 promotes oral squamous cell progression by sponging miR-143-3p. However, the exact function possessed by lncRNA INHBA-AS1 in CRC development remains unclear.

The expression level of INHBA-AS1 in CRC tissues and cell lines was determined by qRT-PCR. The functional role of INHBA-AS1 in CRC was investigated by a series of in vitro assays. RNA immunoprecipitation (RIP), bioinformatics analysis was utilized to explore the potential mechanisms of INHBA-AS1.

The present study identified INHBA-AS1 as a kind of lncRNA with high expression in CRC tissues and cells. Functionally, NHBA-AS1 downregulation in CRC cells suppressed CRC cell proliferation as well as colony formability. Mechanistically, INHBA-AS1/miR-422a/AKT1 established the ceRNA network to regulate MMP-2, -7, -9 expressions that participated the modulation of CRC progression.

In summary, LncRNA INHBA-AS1 contributes to CRC progression through AKT1 pathway, and provides a new mechanism to regulate CRC development, as well as a potential target for treating CRC.
In summary, LncRNA INHBA-AS1 contributes to CRC progression through AKT1 pathway, and provides a new mechanism to regulate CRC development, as well as a potential target for treating CRC.
MicroRNA-329-3p (miR-329-3p) has been shown to be involved in tumor development. But its role in hepatocellular carcinoma has not been explored. Our study aims to explore the effect and mechanism of miR-329-3p on hepatocellular carcinoma development.

Hepatocellular carcinoma tissues and paired paracancerous specimens from 31 hepatocellular carcinoma patients undergoing surgery were collected. Quantitative real-time polymerase chain reaction and Western blot were employed to measure genes expression at mRNA and protein level. CCK-8 and transwell assays were performed to evaluate hepatocellular carcinoma cells proliferation and migration. Dual-Luciferase reporter gene assay was designed to validate the target gene of miR-329-3p.

Our study showed miR-329-3p expression was significantly lower in hepatocellular carcinoma tissue. Pitavastatin order MiR-329-3p mimic inhibits proliferation and migration of HepG2 cells. By using Dual-Luciferase reporter gene assay, we proved that miR-329-3p inhibited HepG2 cell proliferation and migration by targeting USP22 directly. By up- and downregulation of USP22 expression, we also proved that USP22 can activate the Wnt/β-Catenin pathway, which in turn affected the proliferation and migration of HepG2 cells.

We demonstrated that miR-329-3p can inhibit HepG2 cell proliferation and migration by inhibiting USP22-Wnt/β-Catenin pathway. Our study provides novel insights into the aetiology and potential treatment of hepatocellular carcinoma.
We demonstrated that miR-329-3p can inhibit HepG2 cell proliferation and migration by inhibiting USP22-Wnt/β-Catenin pathway. Our study provides novel insights into the aetiology and potential treatment of hepatocellular carcinoma.
The aim of the study was to illustrate the function of circRNA ZFR in aggravating the development of hepatocellular carcinoma (HCC) by upregulating MAP2K1.

CircRNA ZFR levels in 62 paired HCC and paracancerous species were detected. The influence of circRNA ZFR on clinical data of HCC patients was analyzed. After the overexpression or knockdown of circRNA ZFR, changes in viability and clonality of Bel-7402 and Hep3B cells were assessed, respectively. The involvement of circRNA ZFR/MAP2K1 axis in the development of HCC was explored through Luciferase assay and rescue experiments.

CircRNA ZFR was highly expressed in HCC species than the paracancerous ones. Higher level of circRNA ZFR predicted more advanced tumor grading of HCC. The knockdown of circRNA ZFR attenuated the proliferative ability of HCC cells, while the overexpression of circRNA ZFR obtained opposite results. MAP2K1 level was positively correlated to that of circRNA ZFR. Luciferase assay uncovered that circRNA ZFR can be targeted by MAP2K1 through specific binding sites. In addition, the overexpression of MAP2K1 could reverse the influence of silenced circRNA ZFR on proliferative ability of HCC cells.

CircRNA ZFR is upregulated in HCC and closely linked to tumor grading. It promotes proliferative ability in HCC by upregulating MAP2K1.
CircRNA ZFR is upregulated in HCC and closely linked to tumor grading. It promotes proliferative ability in HCC by upregulating MAP2K1.
To explore the regulatory mechanism of microRNA-4282 (miR-4282) on influencing pancreatic cancer progression by targeting ABCB5.

MiR-4282 and ABCB5 levels in 58 cases of pancreatic cancer and paracancerous tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The influences of miR-4282 on pathological indicators and prognosis in pancreatic cancer patients were analyzed. MiR-4282 overexpression model was established in PANC-1 and BxPC-3 cells by transfection of miR-4282 mimic. Transwell and wound healing assay were conducted to illustrate the role of miR-4282 in influencing cell functions of pancreatic cancer. Bioinformatics analysis and Dual-Luciferase reporter assay were carried out to ascertain the interaction between miR-4282 and ABCB5.

MiR-4282 was downregulated in pancreatic cancer samples. Low level of miR-4282 predicted high incidences of lymphatic metastasis and distant metastasis, as well as poor prognosis in pancreatic cancer patients. Overexpression of miR-4282 remarkably inhibited migratory ability in PANC-1 and BxPC-3 cells. MiR-4282 was targeted by ABCB5 through specific binding sites. In pancreatic cancer tissues, ABCB5 level was negatively correlated to that of miR-4282. Overexpression of ABCB5 could abolish the inhibitory effects of overexpressed miR-4282 on the malignant progression of pancreatic cancer.

MiR-4282 is able to inhibit the migratory ability in pancreatic cancer cells by negatively targeting ABCB5, which may become a promising pancreatic cancer biomarker.
MiR-4282 is able to inhibit the migratory ability in pancreatic cancer cells by negatively targeting ABCB5, which may become a promising pancreatic cancer biomarker.
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