Biochemical and Biophysical Research Communications
BRAF activated non-coding RNA (BANCR) promoting gastric cancer cells proliferation via regulation of NF-κB1
Introduction
Gastric cancer is one of the most common cause of death from cancer worldwide [1]. It has been demonstrated that genetic components and environmental factors contribute to the progression of the gastric cancer [2], [3]. Despite the 5- year relative survival rate is increased to about two times, the survival rate of the patients is still low with less than 30% in United States [4], due to the advanced stage of the disease at the time of diagnosis. Therefore, it is an urgent need to demonstrate the regulatory network underlying the development of gastric cancer to explore the efficient or reliable biomarkers for early diagnosis and targeted therapy.
Long non-coding RNAs (long ncRNAs, lncRNAs), longer than 200 nucleotides, are non-protein coding transcripts [5] with the functions to regulate gene expression at the level of chromatin modification, transcription and post-transcriptional processing [6]. BRAF-activated non-coding RNA (BANCR), a 693-bp lncRNA on chromosome 9 is reported to be involved in malignant melanoma [7], lung carcinoma [8] and papillary thyroid carcinoma [9]. BANCR contributes to the proliferation and migration of tumors, which is a potential marker to explain the pathological physiology of tumor formation and a target site to the treatment of cancers. Recently, Li et al. has demonstrated that high expression of BANCR is an independent unfavorable prognostic factor in gastric cancer patients [10]. Even so, very few reports have been demonstrated in gastric cancer. In addition, the mechanism of BANCR underlying gastric cancer is needed to be deeply explored.
MicroRNAs (miRNAs) are small non-coding RNA molecules acting as RNA silencing and post-transcriptional regulation of gene expression. MiR-9 has been demonstrated to play a critical role in the proliferation, invasion and metastasis of various cancers [11], [12], [13], including gastric cancer [14], [15]. The NF-κB1 (P50/105) gene takes part in the regulation of immune responses, cell-cycle progression and oncogenesis [16], [17]. In addition, NF-κB1 expression has been indicated to be mediated by miR-9 in cancers [18], [19]. In present study, we speculated that BANCR probably was involved in the development of gastric cancer cells via NF-κB1 regulation mediated by miR-9.
Section snippets
Specimen collection
Thirty pairs of gastric specimen, including thirty human gastric adenocarcinoma tissues and thirty adjacent tissues, were obtained from the Affiliated Hospital of Jining Medical University. This study was approved by the Ethics Committee of Affiliated Hospital of Jining Medical University. Written informed consents were obtained from all participants.
Cell culture
Human gastric cancer cell lines BGC823 and SGC7901 were purchased from the Type Culture Collection of the Chinese Academy of Sciences (Shanghai,
BANCR expression was up-regulated in gastric cancer
The BANCR expression was first investigated in gastric cancer. As shown in Fig. 1A, the BANCR level in human gastric cancer tissue was almost 5 folds of matched normal gastric tissue. In gastric cancer cells, the elevated BANCR expression was also observed in BGC-823 and MGC-803 cells compared with GES-1 cells (Fig. 1B).
The effects and mechanism of BANCR expression on gastric cancer cell proliferation and apoptosis
To demonstrate the role of BANCR in gastric cancer cell proliferation and apoptosis, a shRNA-323 (LV-BANCR-323) or shRNA-540 (LV-BANCR-540) was transfected into BGC-823 and
Discussion
lncRNAs are newly recognized regulators involved in the human pathophysiologic processes, including oncogenesis [20], [21]. The researches about the mechanisms of lncRNAs on onset and development of diseases are severely limited. In present study, we found that the BANCR expression level was highly expressed in gastric cancer tissues and gastric cancer cells, and miR-9 mediating NF-κB1 participated in the proliferation of cancer cell by BANCR regulation.
BANCR has been indicated to be abnormally
Conflict of interest
All authors declare that there is no conflict of interest.
Acknowledgment
This work is funded by 973 Program (2011CB504302), National Nature Science Foundation of China (30872318) and Scientific and Technological Development Plan of Shandong Province (2010GW20237).
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