Long Intergenic Non-coding RNA Research Articles

Research progress of LincRNA-p21 in tumors

Long-chain non-coding RNA (LncRNA) has more than 200 nucleotides in length and cannot encode proteins. It has a variety of biological functions. A large number of studies have shown that LncRNA is closely related to the occurrence and development of cancer. Researches at the level of molecular biology have found that LncRNA acts as an important regulatory molecule involved in the whole process of life activities and plays a regulatory role in various diseases and tumors. LincRNA-p21 is a novel LncRNA that acts as a translational inhibitor by targeting mRNA or by directing the chromatin site of a protein-binding partner. LincRNA-p21 is closely related to a variety of tumors and exerts its biological functions of carcinogenesis or tumor suppression through different pathways. In this paper, the research progress of the tumor-associated gene LincRNA-p21 was reviews Key words: Non-coding RNA; Long intergenic non-coding RNA; LncRNA-p21; Tumor

Effects of long intergenic non-coding RNA FEZF1-AS1 on proliferation and invasion of gastric cancer cells SGC-7901

Objective To investigate the effects of long intergenic non-coding RNA (Linc) FEZF1-AS1 on proliferation and invasion of SGC-7901 cells. Methods The SGC-7901 cells were classified into two groups: FEZF1-AS1 small interfering RNA (si-FEZF1-AS1) and the negative control siRNA (si-NC). Linc FEZF1-AS1 was knocked down in si-FEZF1-AS1 group by small interfering RNA (siRNA). The proliferative activity of SGC-7901 cells was determined by colony formation assay and cell counting kit-8 (CCK-8) assay, and the invasion ability was studied by wound healing assay and Transwell assay. The expression levels of epithelial-mesenchymal transition (EMT)-related molecules was detected by RT-PCR and Western blotting. Results The results of colony formation assay showed that the colony-forming capacity was impaired in si-FEZF1-AS1 group compared to the si-NC group [(26.78±3.34)% vs. (43.22±4.35)%, t=5.194, P=0.007]; CCK-8 results revealed that the proliferation of SGC-7901 cells was dramatically inhibited in si-FEZF1-AS1 group after 3 days [(31.32±4.48)% vs. (13.86±0.64)%, t=11.590, P=0.000]; Scratch tests showed that, 48 h after scratches in SGC-7901 cells, the space between scratches was significantly increased as compared with that in si-NC group [(598.67±18.81) vs. (428.32±13.90) μm, t=12.620, P=0.000]; The results of Transwell assay also indicated that the number of metastatic cells in the si-FEZF1-AS1 group was significantly decreased compared to the si-NC group [(60.50±5.13) vs. (103.50±9.54), t=7.942, P=0.001]; The results of RT-PCR showed that the relative mRNA expression levels of E-cadherin were increased in si-FEZF1-AS1 group [(2.01±0.36), t=5.435, P=0.002], and those of Vimentin and β-catenin were decreased [(0.54±0.05), t=9.734, P=0.000; (0.50±0.10), t=8.019, P=0.000]. The results of Western blotting revealed that the expression levels of E-cadherin in si-FEZF1-AS1 group were significantly increased as compared with the si-NC group [(86 304±447) vs. (35 623±227), t=175.100, P=0.000], and those of Vimentin and β-catenin in the si-FEZF1-AS1 group were significantly decreased as compared with the si-NC group [(29 135±89) vs. (82 253±353), t=252.800, P=0.000; (15 283±147) vs. (42 506±245), t=165.200, P=0.000]. Conclusion Dysregulation of Linc FEZF1-AS1 can suppress proliferation and invasion of SGC-7901 cells, which may be related to the Wnt/β-catenin signaling pathway. Key words: Gastric cancer; Long intergenic non-coding RNA; Proliferation; Invasion

Effects of long intergenic non-coding RNA 00152 on proliferation and apoptosis of colorectal cancer cells

Objective To study the expression of long intergenic non-coding RNA 00152 (Linc00152) in colorectal cancer (CRC) and cell lines. To investigate the effect of Linc00152 on proliferation and apoptosis of CRC cells. Methods The expression levels of Linc00152 in 31 CRC tissues and adjacent normal tissues, four CRC cell lines (CCL244, SW480, HT29, LoVo) were detected by real-time quantitative polymerase chain reaction(Real-time PCR). Linc00152 was knockdown in CCL244 and HT29 by small interfering RNA (siRNA). Methyl thiazolyl tetrazolium (MTT) assay and clone formation assay were conducted to evaluated the cell proliferation, flow cytometry was used to evaluated the apoptosis. Results Real-time PCR showed that the expression of Linc00152 in CRC tissues (4.18±3.43) was 27.07 times higher than that in the adjacent normal tissues (8.94±3.07, P=0.045). Linc00152 was highly expressed in CRC cell lines. Linc00152 was efficiently down-regulated by siRNA. Inhibition of Linc00152 in CCL244 cells impaired the colony-forming capacity [(26.67±0.47)% vs. (44.67±1.89)%, P=0.006]. MTT assay revealed that the cell viability of CCL244 and HT29 was inhibited in siRNA group [72 h: CCL244 (23.48±3.49)%, HT29 (12.53±2.86)%, P=0.001]. Down-regulation of Linc00152 in CCL244 and HT29 cells induced cells apoptosis [CCL244 (9.08±0.22)% vs. (4.15±0.29)% (P=0.003), HT29 (16.36±0.70)% vs. (7.11±0.88)%, P=0.007]. Conclusion The expression of Linc00152 was high in CRC. Loss of Linc00152 can inhibit cell proliferation and promote cell apoptosis in CRC cells. Key words: Colorectal cancer; Long non-coding RNA; Long non-coding RNA 00152; Proliferation; Apoptosis

Dysregulated Expression of Long Intergenic Non-coding RNAs (LincRNAs) in Urothelial Bladder Carcinoma.

Long intergenic non-coding RNA (lincRNA) has been introduced as key regulators of diverse biological processes, including transcription, chromatin organization, cell growth and tumorigenesis. With regard to the potential role of lincRNAs in cancer development, one may postulate that differential expression of lincRNAs could be employed as a tool in cancer diagnosis, prognosis, and targeted therapy. In this study, we aimed to explore the putative correlation between the expression levels of two lincRNAs: LINC00152 and LINC01082 in the bladder cancer (BC), in comparison with its adjacent non-cancerous tissue. Fifty Iranian subjects diagnosed with BC, representing in different stages and grades participated in this study The mRNA expression levels of the abovementioned lincRNAs were comparatively analyzed in cancerous and their adjacent non-cancerous counterpart tissues, of each subject by Real-Time PCR. The expression levels of LINC00152, and LINC01082 were significantly lower in tumor tissues in comparison with their adjacent normal tissues (P<0.001). More notably, in the case of LINC01082 the reduced expression was differentiated by the muscle invasiveness pattern of the tumor (P= 0.05). Our study presents a new finding about the tumor suppressor potentiality of these lincRNAs in BC development that in turn may suggest them as candidate biomarkers. Replicating this study in higher number of BC subjects, coupled with functional analysis, is necessary to investigate interconnections between these RNAs and cancer development, leading to better understanding of cancer biology.

Integrative genome-wide expression and promoter DNA methylation profiling identifies a potential novel panel of ovarian cancer epigenetic biomarkers

To identify epigenetic-based biomarkers for diagnosis of ovarian cancer we performed MeDIP-Chip in A2780 and CaOV3 ovarian cancer cell lines. Validation by Sequenom massARRAY methylation analysis confirmed a panel of six gene promoters (ARMCX1, ICAM4, LOC134466, PEG3, PYCARD & SGNE1) where hypermethylation discriminated 27 serous ovarian cancer clinical samples versus 12 normal ovarian surface epithelial cells (OSE) (ROC of 0.98). Notably, CpG sites across the transcription start site of a potential long-intergenic non-coding RNA (lincRNA) gene (LOC134466), was shown to be hypermethylated in 81% of serous EOC and could differentiate tumours from OSE (p<0.05). We propose that this potential biomarker panel holds great promise as a diagnostic test for high-grade (Type II) serous ovarian cancer.