&lt;p&gt;SNHG3 Knockdown Suppresses Proliferation, Migration and Invasion, and Promotes Apoptosis in Non-Small Cell Lung Cancer Through Regulating miR-216a/ZEB1 Axis&lt;/p&gt;

Zhou

2021

Preprint

Background and purpose: Thyroid hormone receptor interacting protein 13 (TRIP13) which plays a carcinogenic role in tumors belongs to AAA+ ATPase superfamily. Zinc finger E-box binding homeobox 1 (ZEB1) and epithelial cadherin (E-cad), the key biomarkers of epithelial-mesenchymal transition (EMT), which aberrant expression may promote tumor invasion and metastasis. The purpose of this study is to investigate the expression of TRIP13, ZEB1, and E-cad in infiltrating urothelial carcinoma of bladder (IUCB) and their clinicopathological significance.Methods: The expression of TRIP13, ZEB1, and E-cad in 150 cases of IUCB samples were investigated by immunohistochemistry. Clinicopathological, demography, and follow-up data were also collected.Results: Positive rates of expression of TRIP13 and ZEB1 were significantly higher in IUCB samples when compared with the control bladder samples. And positive rate of expression of E-cad was significantly lower in IUCB than its expression rate in the control group. The positive expression of TRIP13 and ZEB1 were positively associated with tumor stages, local lymph node metastasis (LNM), and tumor node metastasis (TNM) stages. And E-cad expression was negatively associated with tumor stages, LNM, and TNM stages. The results of Kaplan-Meier analysis demonstrated that the patients with TRIP13 and ZEB1 positive expression had an unfavorable overall survival (OS) time when compared with patients with TRIP13 and ZEB1 negative expression. And patients with E-cad positive expression had a favorable OS time when compared with patients with E-cad negative expression. The COX regression analysis indicated that TRIP13, ZEB1, and E-cad, tumor stages, as well as TNM stages were independently factors for OS time in IUCB patients with postoperative therapy.Conclusions: TRIP13, ZEB1, and E-cad may be considered as potentially promising biomarkers for IUCB patients’ prognosis.

Section: Discussionsupporting

confidence: 93%

Expression of TRIP13, ZEB1, and E-cad in Infiltrating Urothelial Carcinoma of Bladder and Their Clinical Significance

Dai

Zhou

2021

Preprint

“…Recent studies have also found that SNHG3 promotes the proliferation and metastasis of non-small cell lung cancer cells by competing with other miRNAs (miR-340-5p and miR-216a-5p). 26 , 27 These data also confirm the important regulation of SNHG3 in non-small cell lung cancer cells, and the SNHG3/miR-515-5p/SUMO2 we found may be only the tip of the iceberg of SNHG3 regulatory network.…”

Section: Discussionsupporting

confidence: 79%

LncRNA SNHG3 Promotes Proliferation and Metastasis of Non-Small-Cell Lung Cancer Cells Through miR-515-5p/SUMO2 Axis

Gao

Technol Cancer Res Treat

et al. 2021

Lung cancer is a global disease and a major cause of cancer-related mortality worldwide. Accumulated studies have confirmed the essential role of long non-coding RNAs (lncRNAs) in the occurrence and development of cancers. Meanwhile, there have been reports concerning the role of Small Nucleolar RNA Host Gene 3 (SNHG3) in various cancers. However, there are so far few studies on the function and mechanism of SNHG3 in lung cancer. In the present study, SNHG3 was found to be highly expressed in lung cancer tissues and cells. Downregulation of SNHG3 could inhibit cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process. In addition, SNHG3 was found to have the ability to bind to miR-515-5p. Furthermore, Small Ubiquitin Like Modifier 2 (SUMO2) was identified to be the downstream target of miR-515-5p, which was negatively correlated with miR-515-5p expression. SNHG3 could positively regulate SUMO2 expression by sponging miR-515-5p. In addition, the rescue experiment showed that simultaneous transfection of miR-515-5p or SUMO2 siRNA could reverse the effect of SNHG3 expression on cell proliferation and metastasis. Collectively, our study demonstrates that SNHG3 can act on miR-515-5p in the form of competitive endogenous RNA (ceRNA) to regulate SUMO2 positively and thus affect the proliferation and metastasis of NSCLC cells. Findings in our study support that SNHG3/miR-515-5p/SUMO2 regulatory axis may become a potential therapeutic target for lung cancer.

“…For example, SNHG3 promoted hepatocellular tumorigenesis by regulating miR-326 expression [ 21 ], and SNHG3 modulated the miR-384/WEE1 G 2 checkpoint kinase axis to regulate laryngeal carcinoma cell proliferation and migration [ 22 ]. In addition, the lncRNA SNHG3 was reported to play a vital role in LUAD progression [ 23 , 24 ]. However, to the best of our knowledge, the tumorigenic properties and underlying mechanism of action of SNHG3 in LUAD progression remain to the determined.…”

Section: Discussionmentioning

confidence: 99%

The Effect of lncRNA SNHG3 Overexpression on Lung Adenocarcinoma by Regulating the Expression of miR-890

Kang

Qiu

Journal of Healthcare Engineering

2021

The lncRNA small nucleolar host gene 3 (SNHG3) was discovered to play an important role in the occurrence and development of lung adenocarcinoma (LUAD). However, the underlying molecular mechanism of SNHG3 in LUAD remains unclear. In the present study, SNHG3 expression levels in LUAD tissues and cell lines were analyzed using reverse transcription-quantitative PCR. The effects of SNHG3 on the proliferation, apoptosis, migration, and invasion of LUAD cells were determined using Cell Counting Kit-8, colony formation, flow cytometry, wound healing, and Transwell chamber assays, respectively. The specific underlying mechanism of SNHG3 in LUAD was investigated using bioinformatics analysis and a dual luciferase reporter assay. The results revealed that SNHG3 expression levels were downregulated in LUAD tissues and cell lines. Functionally, SNHG3 overexpression suppressed the proliferation, migration, and invasion of LUAD cells, while promoting apoptosis. Mechanistically, microRNA- (miR-) 890 was identified as a potential target of SNHG3, and its expression was negatively regulated by SNHG3. Notably, SNHG3 was found to promote LUAD progression by targeting miR-890. In conclusion, the findings of the present study revealed that lncRNA SNHG3 promoted the occurrence and progression of LUAD by regulating miR-890 expression.