TSR2 Induces laryngeal cancer cell apoptosis through inhibiting NF‐κB signaling pathway

He, Hongchao; Han, Bing; Liu, Guijun

doi:10.1002/lary.27035

Cited by 10 publications

(8 citation statements)

References 27 publications

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“…GNL3L has been reported to directly bind to and stabilize MDM2 protein, however its role in PCa has not been studied 37 . TSR2 is known to enhance apoptosis by suppressing NF-kB signaling in laryngeal cancer 38 . The genes listed above potentially influence PCa development and further functional analysis is warranted.…”

Section: Discussionmentioning

confidence: 99%

12 new susceptibility loci for prostate cancer identified by genome-wide association study in Japanese population

et al. 2019

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Genome-wide association studies (GWAS) have identified ~170 genetic loci associated with prostate cancer (PCa) risk, but most of them were identified in European populations. We here performed a GWAS and replication study using a large Japanese cohort (9,906 cases and 83,943 male controls) to identify novel susceptibility loci associated with PCa risk. We found 12 novel loci for PCa including rs1125927 (TMEM17, P = 3.95 × 10−16), rs73862213 (GATA2, P = 5.87 × 10−23), rs77911174 (ZMIZ1, P = 5.28 × 10−20), and rs138708 (SUN2, P = 1.13 × 10−15), seven of which had crucially low minor allele frequency in European population. Furthermore, we stratified the polygenic risk for Japanese PCa patients by using 82 SNPs, which were significantly associated with Japanese PCa risk in our study, and found that early onset cases and cases with family history of PCa were enriched in the genetically high-risk population. Our study provides important insight into genetic mechanisms of PCa and facilitates PCa risk stratification in Japanese population.

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Section: Discussionmentioning

confidence: 99%

12 new susceptibility loci for prostate cancer identified by genome-wide association study in Japanese population

et al. 2019

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“…In the past decades, a number of molecules, such as TSR2, HSP47, snail, and so on were demonstrated to serve important roles in cellular processes including proliferation, differentiation, metastasis, and tumorigenesis in the prognosis of LSCC. [29][30][31][32][33] Tra2β, one of the human alternative splicing factors, is associated with cancer cell survival and therapeutic sensitivity, 34,35 but the regulatory role and regulatory mechanism of Tra2β in LSCC have remained elusive. In the present study, qRT-PCR and immunohistochemistry assays indicated that Tra2β was significantly upregulated in LSCC tissues compared with adjacent nontumorous tissues.…”

Section: Discussionmentioning

confidence: 99%

Tra2β silencing suppresses cell proliferation in laryngeal squamous cell carcinoma via inhibiting PI3K/AKT signaling

Chen

et al. 2018

The Laryngoscope

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Objectives/Hypothesis Transformer‐2 protein homolog beta (Tra2β) generally plays an important role in various human cancers, but its role and the underlying mechanisms in laryngeal squamous cell carcinoma (LSCC) remained unknown. So this study aimed to assess the clinical significance and regulatory mechanisms of Tra2β in LSCC. Study Design Laboratory analysis. Methods Expression of Tra2β was compared in human LSCC tissue samples and paired adjacent normal tissue samples. The in vitro effects of Tra2β expression in Hep‐2 cells on their proliferation, invasion, and migration were assessed by CCK‐8 assays, Matrigel invasion, and transwell migration assays. In addition, the effects of downregulation of Tra2β on the activation of PI3K/AKT signaling pathway were measured using Western blot analysis. The effect of Tra2β on the growth of tumors was detected in the Hep‐2–injected xenograft models in vivo. Results Reverse‐transcription quantitative polymerase chain reaction analysis and immunochemistry analysis indicated that the increased expression of Tra2β in LSCC was significantly associated with poor differentiation, lymph node metastasis, and advanced clinical stage. In vitro knockdown of Tra2β caused a significant decrease in the proliferation, invasion, and migration of Hep‐2 cells. Tra2β silencing decreased the expression of Bcl‐2 but increased Bax and Caspase‐3 both in mRNA and protein levels. Furthermore, knockdown of Tra2β eliminated the suppressive effects of activation of PI3K/AKT signaling. In vivo knockdown of Tra2β significantly inhibited the tumor growth of Hep‐2–injected xenograft mice. Conclusions The results of the present study demonstrated that knockdown of Tra2β inhibits the proliferation and invasion of LSCC cells, at least partly via inhibiting PI3K/AKT signaling. Level of Evidence NA Laryngoscope, 129:E318–E328, 2019

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“…Although they exhibit differences in their dynamics, they both activate the NF-κB pathway (44). Numerous studies (45)(46)(47) have shown that NF-κB transcription factors are adapted to adjust the expression of genes that control cell survival and proliferation. Moreover, deviated activation of the NF-κB signaling is associated with the propagation of many cancers (48,49).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of ectodysplasin‑A receptor‑associated adaptor protein exerts a tumor‑suppressive effect in tongue squamous cell carcinoma cells

Bai

Han

et al. 2020

Exp Ther Med

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Tongue squamous cell carcinoma (TSCC) is a common malignancy in oral cancer with a high mortality and morbidity. The ectodysplasin-A receptor-associated adaptor protein (EDARADD) is a death domain-containing adaptor protein that interacts with the TNF family ligand ectodysplasin A receptor. It is known that EDARADD has an effect on the development of ectodermal derivative tissues, such as hair and teeth. EDARADD expression is also associated with the development of melanoma. However, the role of EDARADD in TSCC remains unknown. The aim of the present investigation was to explore whether EDARADD plays a role in the biological function of TSCC. Immunohistochemistry was used to measure the expression of EDARADD in TSCC tissues and adjacent normal tissue. EDARADD was knocked down in a TSCC cell line in vitro using a specific lentivirus. The expression level of the EDARADD gene and the efficacy of gene knockdown were evaluated by reverse transcription-quantitative PCR, while EDARADD protein expression and the expression levels of Bcl-2, MYC and NF-κBp65 were determined by western blotting. Additionally, MTT assays, colony formation assays and apoptosis assays were carried out to examine the effect of EDARADD knockdown on the TSCC cells. A previous study showed that the majority of the TSCC tissues that were tested had high EDARADD expression. The expression of EDARADD both at mRNA and protein levels was significantly lower (P<0.01) after the gene was knocked down in the CAL27 cells compared with the level in control cells. Downregulation of EDARADD expression inhibited colony formation and proliferation and induced apoptosis of CAL27 cells when compared to control cells (P<0.01). Taken together, these results suggested that EDARADD may be actively involved in the progression of TSCC and that EDARADD may be a novel therapeutic target for the treatment of TSCC.

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TSR2 Induces laryngeal cancer cell apoptosis through inhibiting NF‐κB signaling pathway

Abstract: NA. Laryngoscope, 128:E130-E134, 2018.

Cited by 10 publications

References 27 publications

12 new susceptibility loci for prostate cancer identified by genome-wide association study in Japanese population

12 new susceptibility loci for prostate cancer identified by genome-wide association study in Japanese population

Tra2β silencing suppresses cell proliferation in laryngeal squamous cell carcinoma via inhibiting PI3K/AKT signaling

Knockdown of ectodysplasin‑A receptor‑associated adaptor protein exerts a tumor‑suppressive effect in tongue squamous cell carcinoma cells

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