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Background and purpose: Long non-coding RNA (lncRNA) has been found to be dysregulated in breast cancer and is closely related to the malignant behavior of tumors. This study aimed to explore the effects of LINC02163 targeting miR-338-3p on the proliferation, invasion and migration of breast cancer cells. Methods: Breast cancer tissue samples and the adjacent tissue samples (2 cm to cancer tissue) were collected from 9 female breast cancer patients admitted to People’s Hospital of Zhengzhou from January 2020 to September 2021. Real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) was used to detect the expression of LINC02163 in tissue samples, human normal breast epithelial cell line (MCF-10A) and breast cancer cell lines (MCF-7, BT-20, MDA-MB-231, T47D). MDA-MB-231 was divided into control group, sh-NC group, sh-LINC02163 group, sh-LINC02163+inhibitor-NC group and sh-LINC02163+miR-338-3p inhibitor group. MTT method, transwell test and scratch test were used to detect the MDA-MB-231 cell viability, invasion and migration ability. Western blot was used to detect the protein expression of c-Myc, matrix metalloproteinase (MMP) 2, MMP9, E-cadherin and N-cadherin in MDA-MB-231 cells. Dual luciferase reporter gene was used to detect the targeting relationship between LINC02163 and miR-338-3p. In vivo tumor formation experiment was used to detect tumor volume and weight in nude mice. Immunohistochemical method was used to detect the Ki-67 proliferation index in tumor tissues of BALB/c nude mice. Results: Compared with adjacent tissues, the expression of LINC02163 in breast cancer tissues was significantly higher (P0.05), the cell survival rate, number of invasive cells, migration rate, expressions of c-Myc, MMP2, MMP9 and N-cadherin, tumor volume and weight, and Ki-67 proliferation index were significantly increased, while the expressions of miR-338-3p and E-cadherin were significantly reduced (P

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Objective To investigate the expression of long non-coding RNA LINC02163 in hepatocellular carcinoma (HCC) tissues and HCC cell lines, and its effect on the migration and invasion of hepatocellular carcinoma cells. Methods The differential expression level of LINC02163 in 5 HCC cell lines (HuH-7, HCCLM3, MHCC-97H, SNU-182 and SMMC-7721), normal liver cell line (L02) and 60 HCC tissues and paired adjacent tissues was determined by quantitative real-time PCR (qRT-PCR), and the relationship between its expression level and the clinicopathological parameters of HCC patients was analyzed. LipofectamineTM 2000 was used to transfect LINC02163 small interfering RNA (siRNA) into HCC HuH-7 and HCCLM3 cells in order to knockdown the expression. Then the changes of migration and invasion ability of HCC cells after the knock-down of LINC02163 were examined by Transwell assay. Results The expression level of LINC02163 in HCC tissues was significantly higher than that in paired adjacent tissues (P < 0.001), and the level was significantly correlated with TNM stage and microvascular invasion (MVI) in the patients (all P < 0.01). Compared with normal liver cell line (L02), LINC02163 was highly expressed in 5 HCC cell lines (P < 0.001), among which HuH-7 cells had the highest expression level, followed by HCCLM3 cells. LINC02163 knock-down significantly reduced the migration and invasion abilities in HuH-7 and HCCLM3 cells (P < 0.01). Conclusion LINC02163 is up-regulated in HCC tissues and cell lines and promotes the migration and invasion of HCC cells, which may be closely associated with the occurrence and development of HCC.

Long non-coding RNAs and microRNAs are functional regulators in tumour progression. Herein, we revealed the level LINC02163 was up-regulated in CRC tissues and cell lines, and the expression of LINC02163 negatively correlated with prognosis of CRC patients. Functional experiments demonstrated knockdown of LINC02163 significantly attenuated CRC cells proliferation and metastasis. Mechanism analysis showed miR-511-3p could bind LINC02163 and AKT3, and the expressional level of miR-511-3p negatively correlated with the abundance of LINC02163 and AKT3. Inhibition of LINC02163 suppressed cell proliferation, while transfection of miR-511-3p inhibitor or AKT3 in LINC02163-depletion cells restored cell growth and abolished the cell cycle arrest in G0/G1 phase. Therefore, it was indicated that LINC02163 exerted pro-tumour effect through miR-511-3p/AKT3 axis and was prognostic marker for colorectal cancer.

Recently, long non-coding RNAs (lncRNAs) were involved in promoting gastric cancer (GC) initiation and progression. In the current study, we revealed that the expression level of LINC02163 was elevated in GC cell lines and tissues. Knockdown of LINC02163 inhibited GC cells growth and invasion both in vitro and in vivo. Mechanismly, LINC02163 exerted as a ceRNA and negatively regulated miR-593-3p expression. In addition, FOXK1 was identified as a down-stream target of miR-593-3p. The miR-593-3p/FOXK1 axis mediated LINC02163's effect on GC. To the best of our knowledge, our findings provided the first evidence that LINC02163 functioned as an oncogene in GC. LINC02163 may be a candidate prognostic biomarker and a target for new therapies in GC patients. [ABSTRACT FROM AUTHOR]