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Bladder cancer is one of the most common malignancies of the urinary tract and can be divided into non-muscle-invasive bladder cancer (NMIBC) and muscle-invasive bladder cancer (MIBC). Emerging evidence demonstrates that long noncoding RNAs play a crucial role in the carcinogenesis and progression of bladder cancer. Long intergenic noncoding RNAs (lincRNAs) are a subgroup of long noncoding RNAs (lncRNAs) that do not overlap protein-coding genes. Small nucleolar RNAs (snoRNAs) are a class of noncoding RNAs (ncRNAs) that mainly exist in the nucleolus, are approximately 60–300 nucleotides in length, and are hosted inside the introns of genes. Small nucleolar RNA host genes (SNHGs) have been associated with the origin and development of bladder cancer.
SNHG1, which is located at chromosome 11q12.3, is overexpressed in several types of tumours, including pancreatic, prostate, non-small-cell lung and BLCA . It is widely considered an oncogene that promotes cancer proliferation, migration, invasion and tumorigenesis. SNHG1 can bind and coregulate with the PP2A catalytic subunit (PP2A-c) to promote c-Jun phosphorylation. Then, activated c-Jun increases matrix metalloproteinase 2 (MMP2) transcription, which induces cancer cell invasion and metastasis. Additionally, transcription of miR-34a was downregulated by SNHG1 via autophagy, thus maintaining MM2 mRNA stabilization .
SNHG2, which is also known as growth arrest-specific transcript 5 (GAS-5), is located at chromosome 1q25 and acts as a tumour suppressor in multiple cancers . Studies have found that SNHG2 is expressed at low levels in BLCA cells and tissues and that the expression level of SNHG2 is markedly correlated with the clinical characteristics and prognosis of BLCA. High expression of SNHG2 promotes BLCA cell apoptosis and inhibits tumour proliferation. SNHG2 directly interacts with E2F transcription factor 4 (E2F4) and recruits it to the enhancer of the zeste homolog 2 (EZH2) promoter, thereby downregulating transcription of the EZH2 oncogene . In the BLCA cell line HTB-9, SNHG2 sponges miR-21, thus promoting transcription of its downstream gene phosphatase and tensin homolog (PTEN), leading to the downregulation of antiapoptotic proteins and cell cycle-associated proteins, which suppresses proliferation and increases apoptosis of bladder cancer cells . According to previous studies, downregulation of SNHG2 could also directly arrest the cell cycle at the S phase in a cyclin-dependent kinase 6 (CDK6)-dependent manner .
Linc00001, also known as X-inactive specific transcript (XIST), is located on chromosome Xq13.2. It was first found in the process of X chromosome inactivation, which occurs at the early development stage of mammalian females, and was later shown to act as an oncogene and to be upregulated in multiple types of cancers, including BLCA . Recent studies have revealed that XIST can regulate cancer cell progression by acting as a sponge of miRNAs and binding to proteins . Specifically, the expression of XIST was elevated in BLCA tissues and cell lines, including T24, 253J, RT112 and HT-1376. XIST silencing induced the loss of proliferation, metastasis and stemness capability combined with the overexpression of miR-200c and miR-133a in vitro .
Linc00023 is located on chromosome 14q32.2 within the DLK-MEG3 locus and is also widely known as the maternally expressed 3 gene (MEG3). The deregulation of linc00023 was reported to be involved in the progression of various tumours, including meningioma, hepatocellular cancer, breast cancer and BLCA . Similarly, MEG3 can also act as a ceRNA to regulate tumour cell proliferation and apoptosis. In bladder cancer, MEG3 was found to function as a ceRNA for PTEN by competitively binding miR-494, thus repressing the proliferation, migration and invasion and promoting the apoptosis of tumour cells .
Linc00047 is also known as metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and has a length of 8.5 kb. It is located on chromosome 11q13, is involved in the regulation of several molecular signalling pathways and has been shown to be a potential biomarker in bladder cancer, nasopharyngeal carcinoma and osteosarcoma . The expression of MALAT1 was significantly elevated in BLCA tissues and cell lines and was positively correlated with advanced clinical stage and poor prognosis . In addition, MALAT1 sponged miR-101-3p and suppressed the expression of VEGF-C in BLCA 5637 and EJ-M3 cell lines, enhancing cisplatin sensitivity. Furthermore, the knockdown of MALAT1 in cisplatin-resistant 5637 and EJ-M3 cells could reverse drug resistance .
Linc00080, also known as taurine-upregulated gene 1 (TUG1), is located on chromosome 22q12 and is almost twice as elevated in bladder tissues compared to adjacent normal tissues. It is broadly considered an oncogene in several tumours, such as colorectal cancer, oesophageal cancer, osteosarcoma and bladder cancer . In BLCA, TUG1 is involved in tumour proliferation, metastasis and apoptosis, as well as radioresistance and chemotherapy resistance . Silencing TUG1 in BLCA cell lines restrains the tendency of EMT by acting as a ceRNA of ZEB2 by sponging miR-145 and leading to radioresistance . It also promotes the expression of high mobility group box 1 protein (HMGB1), thus enhancing bladder cancer radioresistance in vivo and in vitro, yet the mechanism needs further exploration .
Linc00178 is located on 19p13.12 and was first identified in bladder transitional cell carcinoma; thus, linc00178 is also known as urothelial cancer associated 1 (UCA1). Recent studies have verified the overexpression and oncogene functions of UCA1 in different tumours . Specifically, UCA1 can serve as a sponge of miRNAs to regulate tumour growth, metastasis, drug resistance and mitochondrial functions. Li et al. found that knockdown of UCA1 in the BLCA cell line 5637 decreased mitochondrial DNA copy number by more than half with accompanying decreased ATP production. The results of a UCA1 overexpression experiment on the BLCA cell line UMUC2 were highly consistent with those of the knockdown experiments.
Linc00319 is a novel lncRNA located on chromosome 21q22.3 that has been implicated in the tumorigenesis and progression of cervical cancer, gastric cancer, osteosarcoma and laryngeal squamous cell carcinoma in a miRNA-dependent manner . Moreover, linc00319 expression levels were remarkably higher in BLCA tissues than in adjacent normal tissues. Patients with higher linc00319 levels had higher clinical stages and lower recurrence-free survival rates .
Linc00355 is located on chromosome 13q21.31 and has been validated to function as a ceRNA by sponging miRNAs in lung squamous cell carcinoma, glioma and hepatocellular carcinoma . In BLCA, linc00355 could act as a sponge of miR-424-5p to modulate high mobility group AT-hook 2 (HMGA2) expression, which could regulate the EMT-related proteins ZEB1, E-cadherin and vimentin and finally contribute to BLCA EMT and lung metastasis .
Linc00649 is located on 21q22.11 and is widely considered an oncogene in multiple tumours, such as lung squamous cell carcinoma, breast cancer and gastric cancer . A recent study found that linc00649 is a basement membrane-related lncRNA and is correlated with clinical prognosis based on analysis of transcriptional and clinical data of bladder cancer from the TCGA, GEO and BM-BASE databases, revealing that linc00649 is a potential biomarker of BLCA. Additionally, a model containing eight lncRNAs, including linc00649, was constructed and used to accurately predict the prognosis of BLCA patients .
Linc00958 is located on 11p15.3 and was found to be substantially expressed in bladder cancer tissues compared to normal bladder epithelial tissues. Increasingly, studies have demonstrated that linc00958 is involved in the malignant progression of various cancers, such as hepatocellular carcinoma, colorectal cancer, osteosarcoma and endometrial cancer . Anna et al. identified 72 BLCA tissues and 8 normal bladder epithelial tissues by RNA sequencing and selected five significantly dysregulated lncRNAs, including linc00958, for further analysis. They found that the knockdown of linc00958 led to a loss of cell mobility in vitro.