Long Noncoding RNA (lncRNA) Small Nucleolar RNA Host Gene 16 (SNHG16) Predicts Poor Prognosis and Sorafenib Resistance in Hepatocellular Carcinoma

Abstract

Background Long noncoding RNAs (lncRNAs) play important roles in cancer development and therapeutic resistance. However, the role of small nucleolar RNA host gene 16 (SNHG16) in the development of hepatocellular carcinoma (HCC) remains largely unknown. Material/Methods In situ hybridization (ISH) staining was performed to detect the expression level of SNHG16 in HCC tissues and adjacent non-cancerous tissues. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the level of SNHG16 in HCC samples, adjacent non-cancerous tissues and HCC cell lines. Transwell assay was performed to investigate the migration and invasion ability of HCC cells. Cell viability assays were performed to determine the ability of proliferation and sorafenib resistance of HCC cells. Results We found that SNHG16 was upregulated in HCC tissues and cell lines and that it was negatively correlated with survival time in HCC patients. Univariate and multivariate analyses revealed that SNHG16 was a significant and independent predictor for the overall survival of HCC patients. Furthermore, downregulation of SNHG16 inhibited proliferation, migration, invasion, and sorafenib resistance in hepatocellular carcinoma cell lines. Conclusions Our findings revealed that lncRNA SNHG16 could be used as an oncogene to predict the outcome of hepatocellular carcinoma.

Clinicopathological significance and prognosis of long noncoding RNA SNHG16 expression in human cancers: a meta-analysis

“…shown that patients with elevated expression of SNHG16 had poor OS in comparison with those with low levels [10][11][12][13][14][15][16][18][19][20][21][22][23][24]. Not only in cancer, recent evidence suggests that SNHG16 also has a significant impact on regulating the inflammatory response.…”

<p><em>SNHG16</em>: A Novel Long-Non Coding RNA in Human Cancers</p>

“…15,[18][19][20][21][22][23] Further analysis showed that high expression of SNHG16 is associated with high tumor grade, multiple tumors, macrovascular invasion, large tumor size, and lymph node status, as well as poor diseasefree survival and shorter overall survival. 15,[19][20][21]23 In HCC patients, multivariate analysis identified SNHG16 overexpression as a significant independent predictor of poor prognosis. 20,23 Moreover, there are other studies of SNHG16 and related clinical effects in non-small cell lung cancer (NSCLC), osteosarcoma, glioma, bladder cancer (BC), ovarian cancer (OC), pancreatic cancer (PC), and papillary thyroid cancer (PTC).…”

“…15,[19][20][21]23 In HCC patients, multivariate analysis identified SNHG16 overexpression as a significant independent predictor of poor prognosis. 20,23 Moreover, there are other studies of SNHG16 and related clinical effects in non-small cell lung cancer (NSCLC), osteosarcoma, glioma, bladder cancer (BC), ovarian cancer (OC), pancreatic cancer (PC), and papillary thyroid cancer (PTC). SNHG16 expression is significantly upregulated in NSCLC tissues and cell lines.…”

“…17 Recent studies have demonstrated that SNHG16 expression is upregulated in multiple types of tumors. Furthermore, downregulation of SNHG16 in cancer cells inhibits cell proliferation, invasion, and migration; induces apoptosis; and results in decreased N-cadherin and increased E-cadherin, 15,[18][19][20][21][22][23] suggesting that SNHG16 also acts as an oncogenic lncRNA in cancer.…”

Noncoding RNAs in gastric cancer: implications for drug resistance

“…It has been found that ncRNAs are involved in almost all cellular functions, such as proliferation, apoptosis, EMT, autophagy and cell cycle control [16][17][18][19][20]. Multiple ncRNAs acts as oncogenes or tumor suppressor genes during carcinogenesis and can also serve as diagnostic and prognostic markers of cancer patients after certain therapies [21,22]. In gastric cancer, a variety of abnormally expressed ncRNAs were identified to promote tumor progression, radioresistance, chemoresistance and targeted therapy sensitivity [23][24][25][26][27][28].…”