LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

Wu, Xiao; Ma, Jing; Chen, Jian; Huang, Han

doi:10.1186/s12903-019-0924-0

Cited by 16 publications

(8 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vivo experiments of the present study demonstrated that CASC15 suppression hampered ESCC xenograft tumor growth. Consistently, previous studies have demonstrated that CASC15 exerted potential oncogenic effects in multiple types of cancer, including tongue squamous cell carcinoma, nasopharyngeal carcinoma, oral squamous cell carcinoma, bladder cancer, melanoma and cervical cancer ( 9 – 12 , 33 , 34 ).…”

Section: Discussionsupporting

confidence: 85%

“…Additionally, lncRNA LOC100133669 facilitates ESCC cell proliferation by regulating Tim50 ( 8 ). CASC15 is an oncogenic factor that has been identified in several types of cancer, such as tongue squamous cell carcinoma, oral squamous cell carcinoma, melanoma and cervical cancer ( 9 – 12 ). Furthermore, CASC15 expression is upregulated in ESCC ( 13 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Long non‑coding RNA CASC15 facilitates esophageal squamous cell carcinoma tumorigenesis via decreasing SIM2 stability via FTO‑mediated demethylation

et al. 2020

View full text Add to dashboard Cite

Long non-coding RNAs (lncRNAs) are involved in the regulation of esophageal squamous cell carcinoma (ESCC) progression. However, the function and mechanism of lncRNA cancer susceptibility candidate 15 (CASC15) are poorly defined. In the present study, tumor and normal adjacent tissues were collected from 45 patients with ESCC. Expression levels of CASC15, fat mass and obesity-associated (FTO) protein and single-minded 2 (SIM2) were examined via reverse transcription-quantitative PCR and western blot assays. Cell proliferation and apoptosis were evaluated via MTT, flow cytometry and caspase-3 activity assays, respectively. Additionally, an ESCC mouse xenograft model was used to assess the function of CASC15 in vivo . The interaction between FTO and CASC15/SIM2 was analyzed via RNA immunoprecipitation and RNA pull-down assays. The results revealed that CASC15 expression was elevated in ESCC tissues, and patients with ESCC exhibiting high CASC15 expression had a poor prognosis. CASC15-knockdown inhibited ESCC cell proliferation and facilitated apoptosis. Additionally, CASC15-knockdown decreased the growth of ESCC xenograft tumors. CASC15 decreased SIM2 stability via FTO-mediated demethylation. Additionally, FTO loss markedly weakened CASC15-mediated pro-proliferative and anti-apoptotic effects in ESCC cells. SIM2 downregulation weakened the effect of CASC15-knockdown on cell proliferation and inhibited the increase of the apoptotic rate and caspase-3 activity induced by CASC15 depletion in ESCC cells. In conclusion, CASC15 promoted ESCC tumorigenesis by decreasing SIM2 stability via FTO-mediated demethylation.

show abstract

Section: Discussionsupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA CASC15 facilitates esophageal squamous cell carcinoma tumorigenesis via decreasing SIM2 stability via FTO‑mediated demethylation

et al. 2020

View full text Add to dashboard Cite

show abstract

“…36 Wu et al demonstrated that lncRNA CACS15 accelerated the migration and invasion of TSCC cells by down-regulating miR-124. 37 PART1 could mediate the secretion of cytokines and metastasis of tumor cells to affect cancer progression. 15 The expression of PART1 was impeded in glioma tissues and exerted suppressive functions on malignant behavior by targeting miR-190a-3p in glioma cell lines.- 35 Similarly, PART1 was down-regulated in TSCC tissues of patients and a higher level of PART1 was positively correlated with better prognosis.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA PART1 Exerts Tumor-Suppressive Functions in Tongue Squamous Cell Carcinoma via miR-503-5p</p>

Zhao

Yanqing

Cheng

et al. 2020

OTT

View full text Add to dashboard Cite

Background: Tongue squamous cell carcinoma (TSCC) accounts for one-third of oral cancers. Previous studies had reported that lncRNA/miRNA regulated the biological behaviors of different cancer cells. However, the mechanisms of PART1 in regulating tumorigenesis and TSCC development via targeting miR-503-5p had not been studied. Methods: The expressions of PART1 and miR-503-5p in tissues and cultured cell lines were detected by qRT-PCR. StarBase 3.0 was used to predict the binding sites of PART1, then dual-luciferase assay and RNA pull-down assay were executed to confirm whether miR-503-5p was a target of PART1. TSCC cells were co-transfected with PART1-overexpressed plasmid or miR-503-5p mimics in vitro, and the transfection efficiency was evaluated through qRT-PCR. Western blot was performed to assess the expressions of EMT-related proteins. CCK-8 and clone formation assays were conducted to detect cell proliferation, TUNEL assay was used to detect apoptosis, and transwell assay was executed to test migration and invasion. Results: The low PART1 expression and high miR-503-5p expression were found in TSCC tissues and cell lines (CAL-27 and SCC9). PART1 expression was positively correlated with patients' prognosis. The targeting and binding relationship between PART1 and miR-503-5p was confirmed, and overexpressed PART1 diminished the expression of miR-503-5p as well. Moreover, PART1 facilitated apoptosis, inhibited proliferation, invasion and migration of TSCC cells, and these influences were impeded by miR-503-5p overexpression. Conclusion: LncRNA PART1 played a cancer-suppressing role in TSCC by targeting miR-503-5p, which provided a potential target for TSCC treatment.

show abstract

“…Several studies have revealed the dysregulation of lncRNAs in TSCC. [35][36][37] Abnormally expressed lncRNAs may exert tumor-promoting or tumor-inhibiting effects and could participate in the regulation of tumor properties in TSCC. 38,39 Thus, lncRNAs may be novel auxiliary diagnostic and therapeutic targets in TSCC.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

Liu

Zhao

Wang

et al. 2020

OTT

View full text Add to dashboard Cite

Long intergenic non-protein coding RNA 519 (LINC00519) promotes the development of lung squamous cell carcinoma. In this study, we detected the expression of LINC00519 in tongue squamous cell carcinoma (TSCC) and examined its clinical significance. Additionally, the regulatory effects of LINC00519 on behaviors of TSCC tumor cells were explored through functional experiments. Finally, mechanistic studies were performed to elucidate the molecular events underlying the tumor-promoting actions of LINC00519 in TSCC. Materials and Methods: The expression of LINC00519 in TSCC tissues and cell lines was determined using quantitative reverse transcription-polymerase chain reaction. Cell counting kit-8 assay, flow cytometric analysis, cell migration and invasion assays and xenograft tumor model analyses were used to detect TSCC cell proliferation, apoptosis, migration and invasion and in vivo tumor growth, respectively. Mechanistic studies were performed using bioinformatics analysis, RNA immunoprecipitation assay, luciferase reporter assay and rescue experiments. Results: LINC00519 was overexpressed in both TSCC tissues and cell lines. A high LINC00519 level was associated with poor overall survival in patients with TSCC. In vitro, LINC00519 played cancer-promoting roles in TSCC progression by facilitating cell proliferation, migration and invasion and restraining cell apoptosis. In vivo, LINC00519 downregulation resulted in decreased TSCC tumor growth. Mechanistically, LINC00519 acted as a competing endogenous RNA for microRNA-876-3p (miR-876-3p), which directly targets metastasis associated with colon cancer-1 (MACC1), in TSCC cells. LINC00519 upregulated the expression of MACC1 in TSCC cells by sequestering miR-876-3p. Rescue experiments further affirmed that miR-876-3p inhibition or MACC1 overexpression mitigated the inhibitory influences of LINC00519 depletion on cell proliferation, migration and invasion and neutralized the promoting actions of LINC00519 knockdown on cell apoptosis in TSCC. Conclusion: LINC00519 aggravated the oncogenicity of TSCC by regulating the miR-876-3p/MACC1 axis. Our findings suggest that the LINC00519/miR-876-3p/MACC1 pathway may be an underlying therapeutic target in TSCC.

show abstract

LncRNA CACS15 regulates tongue squamous cell carcinoma cell behaviors and predicts survival

Cited by 16 publications

References 15 publications

Long non‑coding RNA CASC15 facilitates esophageal squamous cell carcinoma tumorigenesis via decreasing SIM2 stability via FTO‑mediated demethylation

Long non‑coding RNA CASC15 facilitates esophageal squamous cell carcinoma tumorigenesis via decreasing SIM2 stability via FTO‑mediated demethylation

<p>LncRNA PART1 Exerts Tumor-Suppressive Functions in Tongue Squamous Cell Carcinoma via miR-503-5p</p>

<p>Long Intergenic Non-Protein Coding RNA 519 Promotes the Biological Activities of Tongue Squamous Cell Carcinoma by Sponging microRNA-876-3p and Consequently Upregulating MACC1</p>

Contact Info

Product

Resources

About