BRAF-activated Non-coding RNA Expression Research Articles

Interaction of BANCR in the relationship between Hashimoto's thyroiditis and papillary thyroid carcinoma expression patterns and possible molecular mechanisms.

Previous studies have established a connection between Hashimoto's thyroiditis (HT) and an increased risk of papillary thyroid carcinoma (PTC). However, the molecular mechanisms driving this association are not well understood. The long non-coding RNA (lncRNA) BRAF-activated non-coding RNA (BANCR) has been implicated in various cancers, suggesting a potential role in the HT-PTC linkage. This study investigated the expression levels of BANCR in PTC and HT samples, compared to control tissues. We also examined the association between BANCR expression and clinicopathological features, including lymph node metastasis. Furthermore, we explored the molecular mechanisms of BANCR in PTC pathogenesis and its potential as a therapeutic target. BANCR expression was significantly lower in PTC samples than in controls, while it was moderately increased in HT samples. In PTC cases with concurrent HT, BANCR expression was markedly reduced compared to normal tissues. Our analysis revealed BANCR's role as an oncogene in PTC, influencing various cancer-related signaling pathways. Interestingly, no significant correlation was found between BANCR expression and lymph node metastasis. Our findings underscore the involvement of BANCR in the connection between HT and PTC. The distinct expression patterns of BANCR in PTC and HT, especially in PTC with concurrent HT, provide new insights into the molecular interplay between these conditions. This study opens avenues for the development of innovative diagnostic and therapeutic strategies targeting BANCR in PTC and HT.

STM2457 Inhibits the Invasion and Metastasis of Pancreatic Cancer by Down-Regulating BRAF-Activated Noncoding RNA N6-Methyladenosine Modification.

Pancreatic cancer is a malignant tumor of the digestive system that is highly malignant, difficult to treat, and confers a poor prognosis for patients. BRAF-activated noncoding RNA (BANCR) has been proven to play an important role in the invasion and metastasis of pancreatic cancer. In this study, we focused on BANCR as a potential therapeutic target for human pancreatic cancer. The BANCR level in pancreatic cancer tissues and cells is affected by m6A methylation. Based on this, the aim of our study was to investigate the effect of a highly potent and selective first-in-class catalytic inhibitor of METTL3 (STM2457) on BANCR m6A methylation and its malignant biological behaviors in pancreatic cancer. The relationship between BANCR expression and BANCR m6A modification was detected with RT-qPCR and MeRIP-PCR. The expression of methyltransferase-like 3 (METTL3), the key enzyme involved in m6A methylation, in pancreatic cancer tissues was detected using a Western blot. STM2457 was used in vitro to investigate its resistance to the proliferation, invasion, and metastasis of pancreatic cancer cells. BANCR was overexpressed in pancreatic cancer tissues and cells, which was associated with poor clinical outcomes and validated in pancreatic cancer cell lines. m6A modification was highly enriched within BANCR and enhanced its expression. Remarkably, STM2457 inhibited the proliferation, invasion, and metastasis of pancreatic cancer cells by down-regulating BANCR m6A modifications. This study demonstrates the promise of BANCR as a new diagnostic and therapeutic target for pancreatic cancer and reveals the therapeutic effect that STM2457 exerts on pancreatic cancer by down-regulating BANCR m6A modifications.

Study of LncRNA BANCR Expression in Tumor Tissues and Adjacent Normal Tissues in Gastric Cancer Patients.

Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in various biological processes, including cancer development and progression. This study aimed to investigate the expression differences of the BRAF-activated non-coding RNA (BANCR) gene in GC tissues compared to adjacent normal tissues. The potential diagnostic significance of BANCR in GC was explored, with the aim of improving diagnostic and therapeutic approaches for this global health burden. Tissue samples from 100 gastric cancer (GC) patients were collected, and BANCR expression was analyzed using quantitative real-time PCR. Correlations between BANCR expression and clinicopathological features were assessed, and its biomarker potential was evaluated. In individuals diagnosed with GC, the expression of BANCR was notably elevated in tumor tissues compared to adjacent normal tissues (P < 0.0001). However, the analysis of gene expression data did not demonstrate any statistically significant correlation between elevated BANCR expression and clinicopathological features. According to the ROC analysis, BANCR demonstrated an AUC of 0.6733 (P < 0.0001), with a sensitivity of 73% and a specificity of 45%. However, further evaluation is required to determine its potential as a biomarker (CI 95% = 0.5992 to 0.7473). The observed upregulation of BANCR in GC tissues implies its potential involvement as an oncogenic lncRNA in GC patients. Furthermore, BANCR may serve as a promising biomarker for identification and treatment of GC.

LncRNA BANCR Attenuates the Killing Capacity of Cisplatin on Gastric Cancer Cell Through the ERK1/2 Pathway.

PurposeChemotherapy-based comprehensive treatments are the most important therapeutic methods for patients with advanced gastric cancer, but chemoresistance often cause treatment failure. Long non-coding RNA (LncRNA) BRAF-activated non-coding RNA (BANCR) has been shown to participate in many biological behaviors of multiple cancers. However, the biological roles of LncRNA BANCR in chemoresistance of gastric cancer remain unclear. Here, we aimed to evaluate the functions of LncRNA BANCR on the therapy of gastric cancer.MethodsIn this study, LncRNA BANCR expression was detected in gastric cancer patient samples and cell lines by quantity polymerase chain reaction (qPCR). Cell proliferation and viability in cisplatin-treated cells were measured using clonogenic survival assay and cell counting kit-8. The levels of ERK1/2 pathway molecules were tested with Western blot. Ly3214996, an inhibitor of ERK signal pathway, was administered to assess the effects of BANCR overexpression on gastric cancer cell with cisplatin-treated resistance. Moreover, the role of BANCR in cisplatin resistance of gastric cancer was validated in xenograft mouse models in vivo.ResultsOur study revealed that LncRNA BANCR expression was also significantly increased in gastric cancer tissues compared with adjacent normal tissues. Furthermore, we found that BANCR overexpression promoted gastric cancer cell resistance to cisplatin in vitro. Ly3214996 treatment abolished the BANCR overexpression-mediated gastric cancer cell cisplatin resistance via regulating the phosphorylation of ERK protein. Knock-down of BANCR significantly delayed tumor growth in xenograft mouse models.ConclusionBANCR promoted cisplatin resistance of gastric cancer cells by activating ERK1/2 pathway. Inhibition of BANCR markedly suppressed the growth of gastric cancer cells in vitro as well as in vivo. These results provided a new strategy for gastric cancer therapy via targeting BANCR.

LncRNA BANCR induced vascular smooth muscle cell proliferation by downregulating miR-34c methylation in atherosclerosis.

Aberrant vascular smooth muscle cell (VSMCs) proliferation involves in the development of atherosclerosis. It reported that Long noncoding BRAF-activated noncoding RNA (BANCR) and miR-34c played opposite roles in the regulation of the proliferation of VSMCs, indicating that there might be a potential interaction between them. This study was to investigate the relationship between BANCR and miR-34c in atherosclerosis. Blood (5ml) was obtained from 56 patients with atherosclerosis and 56 healthy volunteers after they were fasted overnight, and plasma was extracted from the blood. Human Aortic Smooth Muscle Cells (HASMCs) were used to perform in vitro cell experiments. RT-qPCR was performed to measure the expression of BANCR and miR-34c in plasma and HASMCs. Dual luciferase reporter assay detected the interaction between BANCR and miR-34c. CCK-8 assay was used to assess the effects of BANCR and miR-34c overexpression on the proliferation of HASMCs. Western blotting was used to assess the effects of BANCR and miR-34c overexpression on the protein expression of HMGB1, TNF-ɑ and Bcl-2. In this study, we found that BANCR was upregulated, while miR-34c was downregulated in atherosclerosis. Bioinformatics analysis showed that BANCR and miR-34c could directly interact with each other. Moreover, overexpression of BANCR could decrease the expression of miR-34c in HASMCs, but overexpression of miR-34c could not affect the expression of BANCR. Furthermore, overexpression of BACNR increased miR-34c methylation, and knockdown of endogenous BANCR decreased miR-34c methylation. In addition, overexpression of BANCR reduced the effects of miR-34c on HASMCs proliferation and reversed the effects of miR-34c on HMGB1, TNF-ɑ and Bcl-2 expression. BANCR overexpression could induce HASMCs proliferation by downregulating the miR-34c methylation. Therefore given BANCR upregulation in atherosclerosis, its expression may be considered as a novel and useful biomarker for atherosclerosis prevention and prognosis. However considering the possible effects of other underlying diseases on both BANCR expression and miR-34c in atherosclerosis, further investigation is suggested for future research.

LncRNA LINC-PINT is downregulated in melanoma and regulates cell proliferation by downregulating lncRNA BANCR.

The development of melanoma may involve long non-coding RNAs (lncRNAs); however, the functions of the majority of lncRNAs in melanoma are unknown. The present study investigated the role of long intergenic non-protein coding RNA p53 induced transcript (LINC-PINT) in melanoma. In the present study, quantitative PCR was used to detect gene expression, overexpression experiments were performed to analyze gene interactions and CCK-8 assays were used to analyze cell proliferation. LINC-PINT was downregulated, while BRAF-activated non-coding RNA (BANCR) was upregulated in melanoma tissues compared with normal adjacent tissues. Expression levels of LINC-PINT decreased, while expression levels of BANCR increased with increasing tumor thickness. The expression levels of LINC-PINT and BANCR were inversely associated in melanoma tissues but not in healthy adjacent tissue. LINC-PINT overexpression downregulated BANCR expression in melanoma cells, while BANCR overexpression did not significantly affect LINC-PINT expression. LINC-PINT overexpression inhibited melanoma cell proliferation in vitro compared to controls. BANCR overexpression attenuated the effects of LINC-PINT overexpression. The present study revealed that lncRNA LINC-PINT is downregulated in melanoma and may regulate melanoma cell proliferation by downregulating lncRNA BANCR.

LncRNA BANCR suppresses cell viability and invasion and promotes apoptosis in non-small-cell lung cancer cells in vitro and in vivo.

Background: As a leading cause of deaths worldwide, lung cancer is a collection of diseases with diverse etiologies which includes non-small-cell lung cancer (NSCLC). Increasing evidence reported that aberrant expression of BRAF activated non-coding RNA (BANCR) was involved in the tumorigenesis and progression of various malignancies.Purpose and methods: However, its role in NSCLC has not been completely clarified. In the present study, we identified the role of BANCR in the regulation of NSCLC cell viability, invasion, and apoptosis. Down-regulation of BANCR expression was significantly observed in different NSCLC cell lines (A549, H1299, H1650, H1975, SPC-A1, and PC-9), tumor tissue from NSCLC mouse model and 30 human NSCLC tissues compared with adjacent normal tissues.Result: Overexpression of BANCR in these six NSCLC cell lines attenuated the cell viability and invasion. An increased apoptotic level caused by BANCR overexpression was also detected and displayed a conversed influence on Bcl-2 and Bax expression in mRNA and protein level. Furthermore, we identified the effect of BANCR overexpression on tumor growth in NSCLC mouse model. The restoration of BANCR expression inhibits NSCLC.Conclusion: Taken together, our findings shed an insight on the novel molecular mechanisms of lung NSCLC oncogenesis and provide the information for new therapeutic approaches on the disease.

Long non-coding RNA BANCR regulates cancer stem cell markers in papillary thyroid cancer via the RAF/MEK/ERK signaling pathway

Thyroid cancer is one of the most common malignant tumors of the endocrine system. Among all thyroid cancers, papillary thyroid carcinoma (PTC) is the most common type. The BRAF-activated non-coding RNA (BANCR) is a 693-bp nucleotide transcript which was first identified in melanoma. However, the role of BANCR in the development of thyroid cancer remains unclear. Therefore, the present study investigated the potential involvement of BANCR in the development of thyroid cancer invitro using patient tissue samples and a panel of thyroid cancer cell lines, and invivo using a xenograft mouse model. We observed that BANCR was expressed at a higher level in human thyroid tumor tissues than that noted in the adjacent normal tissues. The expression level of BANCR differed between cultured thyroid cancer cell lines; BANCR expression was lower in the BCPAP cell line than that observed in the CAL-62, WRO and FTC-133 cell lines. Western blot analysis and flow cytometry revealed that overexpression of BANCR in the BCPAP cell line resulted in increased expression of the cancer stem cell markers, LGR5 and EpCAM. Single-clone formation experiments showed that upregulated expression of BANCR in the BCPAP cell line promoted an increase in the number of clones formed. Similarly, in microsphere formation experiments, overexpression of BANCR resulted in increased number and size of microspheres compared with the control cell line. Western blotting experiments showed that BANCR overexpression in BCPAP upregulated the expression of phosphorylated c-Raf, MEK1/2 and ERK1/2. Inhibition of c-Raf via U0126 decreased the expression of LGR5 and EpCAM, as well as phosphorylated levels of c-Raf, MEK1/2 and ERK1/2 in the BCPAP cells, compared to levels in the DMSO controls. In the xenograft mouse model, BANCR overexpression in the thyroid cancer cells significantly increased tumor growth. Taken together, these results suggest that BANCR plays a role in PTC development by regulating the expression of cancer stem cell markers LGR5 and EpCAM via the c-Raf/MEK/ERK signaling pathway. Therefore, BANCR may be used as a novel prognostic marker for PTC.

Ultrasound reverses adriamycin-resistance in non-small cell lung cancer via positive regulation of BRAF-activated non-coding RNA (BANCR) expression

Objectives: Multi-drug resistance (MDR) remains one of the major obstacles to successful chemotherapy in patients with cancer. BRAF-activated non-coding RNA (BANCR) has been reported to be regulated in non-small cell lung cancer (NSCLC). In the present study, the researchers investigated the effects of ultrasound on BANCR expression, and its possible mechanisms were investigated in vitro and in vivo. Methods: The Adriamycin-resistance of A549/ADM cells and the transplantation tumor model of A549/ADM in nude mice were established. Real-time PCR was used to quantify BANCR expression in cells and in mice examined with or without ultrasound. P-gp and MRP protein expression were measured by western blot. The cell viability was detected by MTT assay. Results: ANCR expression was significantly elevated by ultrasound in A549/ADM cells and tumor tissue from xenograft mice. In in vitro experiments, P-gp and MRP levels were markedly reduced by ultrasound. When the cancer cells up-regulated BANCR by transfection of pCDNA-BANCR, P-gp and MRP levels were inhibited. In addition, the down-regulation of BANCR by si-BANCR transfection elevated their expression. Conclusion: Ultrasound reversed adriamycin-resistance in A549/ADM cells by regulating BANCR expression, and P-gp and MRP regulation were involved in this process.

Upregulation of lncRNA BANCR associated with the lymph node metastasis and poor prognosis in colorectal cancer

BackgroundGrowing evidence has supported that long non-coding RNAs (lncRNAs) could play vital roles in the development, progression, and prognosis of colorectal cancer (CRC). However, little is known about the clinical significance of BRAF-activated non-coding RNA (BANCR) in CRC. The aim of this study is to explore the clinical value of lncRNA BANCR in CRC patients.MethodsThe expression of lncRNA BANCR was measured in 106 CRC tissues and 65 adjacent normal tissues using the quantitative real-time PCR.ResultsThe study showed that lncRNA BANCR was highly expressed in CRC tissues compared with adjacent normal tissues (P < 0.001). In addition, high expression of lncRNA BANCR was positively correlated with the lymph node metastasis (P < 0.001). Kaplan–Meier analysis showed that patients with high lncRNA BANCR expression had a shorter overall survival (OS) compared with the low lncRNA BANCR expression group (P = 0.001). Interestingly, for the group of patients with the lymph node metastasis, we found the similar result that high lncRNA BANCR expression was related to poor OS (P = 0.004). Furthermore, the multivariate Cox regression model analysis indicated that high expression of lncRNA BANCR was an independent poor prognostic factor in CRC patients (HR 2.24, 95% CI 1.22–4.16, P = 0.009).ConclusionsUpregulation of lncRNA BANCR may be associated with the lymph node metastasis and poor survival of CRC. LncRNA BANCR could be served as a novel and useful biomarker for CRC lymph node metastasis and prognosis.

BRAF-activated lncRNA predicts gastrointestinal cancer patient prognosis: a meta-analysis

BRAF activated non-coding RNA (BANCR) is often dysregulated in cancer. We performed a meta-analysis to clarify its functions as a prognostic indicator in malignant tumors. We searched the PubMed, Medline, OVID, Cochrane Library, and Web of Science databases to identify BANCR-related studies. Nine original studies and 898 total patients were included in the meta-analysis. Hazard ratios (HR) and 95% confidence intervals (CI) were extracted from the included studies to determine the relationship between BANCR expression and patient overall survival (OS). Odds ratios (OR) were calculated using RevMan 5.3 software to assess associations between BANCR expression and pathological parameters. High BANCR expression correlated with lymph node metastasis (LNM) (OR = 3.41, 95% CI: 1.82–6.37, P = 0.0001), distant metastasis (DM) (OR = 2.98, 95% CI: 1.76–5.07, P < 0.0001), tumor stage (OR = 3.11, 95% CI: 1.89–5.12, Z = 3.25, P < 0.0001), and poor OS (pooled HR = 1.98, 95% CI: 1.20–3.27, P = 0.008) in gastrointestinal (GI) cancer patients, but not in non-GI cancer patients. Our results support the notion that BANCR as a promising prognostic biomarker in Chinese patients with GI cancer.

Over-expression of long noncoding RNA BANCR inhibits malignant phenotypes of human bladder cancer.

BackgroundAccumulating evidences indicated that lncRNAs play crucial regulatory roles in oncogenesis and progression of cancers. BRAF activated non-coding RNA (BANCR) has been identified to contribute to the progression of some human cancers. However, the relationship between BANCR and bladder cancer (BC) is largely unclear.MethodsBANCR expression levels in BC, paired non-cancer tissues and BC cell lines were detected by real-time quantitative RT-PCR (qRT-PCR). The relationships between BANCR expression levels and the clinical characteristics were evaluated. BANCR expression was enhanced by transfecting a pcDNA-BANCR vector. We used both CCK-8 assay and Edu assay to detect cell proliferation. We also detect cell apoptosis and migration by using ELISA assay, Flow cytometry and transwell assay, respectively. All statistical analyses were executed by using the SPSS 20.0 software.ResultsBANCR expression levels were remarkably decreased in BC tissues compared with adjacent noncancerous tissues. BANCR expression levels in two BC cell lines were also significantly down-regulated. Clinicopathologic analysis revealed that low BANCR expression was positively correlated with TNM stage, but not associated with other clinicopathological characteristics. BANCR has been successfully overexpressed in BC cell lines (T24 and SW780) by transfecting a pcDNA-BANCR vector. Cell proliferation inhibition, apoptosis induction and migration suppression were also observed in pCDNA-BANCR-transfected T24 and SW780 cells.ConclusionsThese data suggested that BANCR represents a tumor suppressor player in bladder cancer, contributes to tumor proliferation, apoptosis and migration, and may serve as a new candidate biomarker and a potential therapeutic target for patients with BC.

Upregulation of the long non-coding RNA BANCR correlates with tumor progression and poor prognosis in esophageal squamous cell carcinoma.

Esophageal squamous cell cancer was one of the most lethal tumors. The lack of effective early diagnosis and treatment ways brings its mortality quite high. Esophageal squamous dysplasia (ESD), is the only histopathology that predicts the development of ESCC. Recent evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in the tumor progression and poor prognosis. BRAF activated non-coding RNA (BANCR) is a 693-bp transcript with a potential functional role in melanoma cell migration. The clinical significance of BANCR, and its' relationship with precancerous lesion of ESCC are unclear. Expression of BANCR was analyzed in 142 ESCC tissues and eight ESCC cell lines using quantitative polymerase chain reaction (qPCR) assays. We further analyzed the BANCR expression level in plasma and precancerous lesion of ESCC. In our results, BANCR levels in plasma were significantly higher in ESCC patients than in normal controls and correlated well with the presence of tumor status. Besides, BANCR expression increased significantly from low to high-grade intraepithelial neoplasia. Additionally, increased BANCR expression was associated with worse histologic grade, advanced TNM stage, more lymph node metastasis, and shorter survival of ESCC patients. The expression level of BANCR reverts to normal after the tumor has been resected, and the expression level of BANCR increased with the disease progression. Increased BANCR expression was found to be an independent prognostic factor for ESCC. In summary, BANCR may be a novel tumor biomarker for early detection, a prospective prognostic indicator and a potential therapeutic target for ESCC and ESD patients.

Increased expression of LncRNA BANCR and its prognostic significance in human hepatocellular carcinoma.

BackgroundLong noncoding RNAs (lncRNAs) have been proved to play important roles in the tumorigenesis and development of human hepatocellular carcinoma (HCC). The aim of our study is to investigate the expression and function of BRAF-activated noncoding RNA (BANCR) in HCC.MethodsBANCR expression was detected in HCC tissues and cell lines by using quantitative real-time PCR (qRT-PCR). Association between BANCR levels and clinicopathological factors and patient prognosis was also analyzed. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), flow cytometry, and transwell invasion and migration assays were used to investigate the role of BANCR in the regulation of biological behaviors of HCC cells.ResultsBANCR expression was remarkably increased in HCC tissues compared with adjacent noncancerous tissues (P < 0.001). BANCR expression in four HCC cell lines was also significantly upregulated (P < 0.05). Clinicopathologic analysis revealed that high BANCR expression correlated with high tumor grade, large tumor size, venous infiltration, advanced tumor, node, and metastasis (TNM) stage, and shorter overall survival. Multivariate regression analysis identified BANCR overexpression as an independent unfavorable prognostic factor (relative risk [RR] 4.245; P = 0.015) in HCC patients. Moreover, BANCR downregulation in Hep3B cells impaired cell proliferation, promoted cell apoptosis, reduced cell invasion and migration, led to downregulated vimentin, and upregulated E-cadherin protein levels.ConclusionsThese findings suggested that BANCR may contribute to HCC initiation and progression and would be used as not only a novel prognostic marker but also a potential therapeutic target for this disease.

Increased expression of the lncRNA BANCR and its prognostic significance in human osteosarcoma.

Long noncoding RNAs (lncRNAs) play important roles in the formation and progression of many types of human malignancies. The aim of our study was to investigate the expression and biological functions of the lncRNA BRAF-activated noncoding RNA (BANCR) in human osteosarcoma. BANCR expression was quantified by real-time PCR in human osteosarcoma cell lines and tissues. We analyzed the association between BANCR levels and clinicopathological factors and patient prognosis. MTT, flow cytometric, and transwell invasion assays were performed to observe the effects of BANCR on MG-63 cell biological behaviors. BANCR overexpression was observed in osteosarcoma cell lines and clinical specimens. Increased BANCR expression was significantly associated with large tumor size, positive distant metastasis, and advanced clinical stage. High BANCR expression in osteosarcoma was an independent predictor of poor survival. Downregulation of BANCR inhibited MG-63 cell proliferation and invasion and promoted cell apoptosis in vitro. These findings suggested that BANCR may act as a tumor promoter in osteosarcoma and could serve as a potential therapeutic target for this disease.

Long Non-Coding RNA BANCR Promotes Endometrial Cancer Cell Proliferation and Invasion by Regulating MMP2 and MMP1 via ERK/MAPK Signaling Pathway

Background/Aims: Microarray screening had found BRAF-activated non-coding RNA (BANCR) was significantly upregulated in type 1 endometrial cancer (EC). This study aimed to assess the potential role of long non-coding RNA (lncRNA) BANCR in the pathogenesis and progression of type 1 EC. Methods: Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to confirm the expression of BANCR in type 1 EC tissue, and analyze its clinical significance. In vitro, RNA interference (siRNA) was used to investigate the biological role of BANCR in type 1 EC. Results: qRT-PCR revealed that the expression of lncRNA BANCR was higher in type 1 EC (P<0.01). BANCR expression was significantly correlated with FIGO stage, pathological grade, myometrial invasion, and lymph node metastasis. The expression of BANCR was significantly correlated with that of MMP2/MMP1. In vitro, knockdown of BANCR significantly suppressed proliferation, migration, and invasion of Ishikawa and HEC-1A cells, and significantly inhibited the ERK/MAPK signaling pathway that decreased MMP2 and MMP1 expression. Conclusion: BANCR is highly expressed in type 1 EC tissue and promotes EC-cell proliferation, migration, and invasion by activating ERK/MAPK signaling pathway that regulates MMP2/MMP1 expression. BANCR is expected to become a prognostic marker and therapeutic target in type 1 EC.

Downregulated Long Noncoding RNA BANCR Promotes the Proliferation of Colorectal Cancer Cells via Downregualtion of p21 Expression.

BRAF activated non-coding RNA (BANCR), a long non-coding RNA (lncRNA), is crucial for cell migration in melanoma cells and non-small cell lung cancer (NSCLC) cells. However, little is known regarding the role of this gene in the proliferation of colorectal cancer. Therefore, we investigated the involvement of BANCR in the proliferation of colorectal cancer cells. In this study, we show that BANCR expression was significantly down-regulated in colorectal cancer tissues compared with normal tissues, and overexpression of BANCR suppressed colorectal cancer cell growth in vitro and in vivo. We also determined that pCDNA-BANCR-mediated colorectal cancer cell proliferation was associated with induction of G0/G1 cell-cycle arrest and apoptosis enhancement through regulation of p21, and its effects were most likely posttranscriptional. Taken together, our findings suggest that down-regulation of BANCR contributes to the proliferation of colorectal cancer cells, at least in part, through the regulation of p21 protein.

Long non-coding RNA BANCR regulates growth and metastasis and is associated with poor prognosis in retinoblastoma.

Recent evidence shows that BRAF-activated non-coding RNA (BANCR) acts as a critical role in the proliferation and metastasis in malignant melanoma and lung cancer; however, little is known about the significance of lncRNA BANCR in retinoblastoma. The purpose of our study is to explore the role of lncRNA BANCR in retinoblastoma clinical samples and cell lines. The expression of lncRNA BANCR was measured in 60 retinoblastoma samples and normal retina samples by using RT-PCR. The effects of lncRNA BANCR on cell proliferation, migration, and invasion were also explored. In our results, lncRNA BANCR is overexpressed in retinoblastoma tissues and cell lines and is associated with tumor size, choroidal invasion, and optic nerve invasion. Moreover, patients with high levels of lncRNA BANCR expression had poorer survival than those with lower levels of lncRNA BANCR expression. Multivariate analysis showed that increased lncRNA BANCR expression was a poor independent prognostic factor for retinoblastoma patients. Furthermore, knocking down lncRNA BANCR expression significantly suppressed the retinoblastoma cell proliferation, migration, and invasion in vitro. In conclusion, lncRNA BANCR plays a significant role in retinoblastoma aggressiveness and prognosis and may act as a promising target for therapeutic strategy and prognostic prediction.

Downregulation of BRAF activated non-coding RNA is associated with poor prognosis for non-small cell lung cancer and promotes metastasis by affecting epithelial-mesenchymal transition

BackgroundRecent evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in the regulation of cellular processes, such as differentiation, proliferation and metastasis. These lncRNAs are found to be dysregulated in a variety of cancers. BRAF activated non-coding RNA (BANCR) is a 693-bp transcript on chromosome 9 with a potential functional role in melanoma cell migration. The clinical significance of BANCR, and its’ molecular mechanisms controlling cancer cell migration and metastasis are unclear.MethodsExpression of BANCR was analyzed in 113 non-small cell lung cancer (NSCLC) tissues and seven NSCLC cell lines using quantitative polymerase chain reaction (qPCR) assays. Gain and loss of function approaches were used to investigate the biological role of BANCR in NSCLC cells. The effects of BANCR on cell viability were evaluated by MTT and colony formation assays. Apoptosis was evaluated by Hoechst staining and flow cytometry. Nude mice were used to examine the effects of BANCR on tumor cell metastasis in vivo. Protein levels of BANCR targets were determined by western blotting and fluorescent immunohistochemistry.ResultsBANCR expression was significantly decreased in 113 NSCLC tumor tissues compared with normal tissues. Additionally, reduced BANCR expression was associated with larger tumor size, advanced pathological stage, metastasis distance, and shorter overall survival of NSCLC patients. Reduced BANCR expression was found to be an independent prognostic factor for NSCLC. Histone deacetylation was involved in the downregulation of BANCR in NSCLC cells. Ectopic expression of BANCR impaired cell viability and invasion, leading to the inhibition of metastasis in vitro and in vivo. However, knockdown of BANCR expression promoted cell migration and invasion in vitro. Overexpression of BANCR was found to play a key role in epithelial-mesenchymal transition (EMT) through the regulation of E-cadherin, N-cadherin and Vimentin expression.ConclusionWe determined that BANCR actively functions as a regulator of EMT during NSCLC metastasis, suggesting that BANCR could be a biomarker for poor prognosis of NSCLC.