Identification of TRA2B-DNAH5 fusion as a novel oncogenic driver in human lung squamous cell carcinoma

Li, Fēi; Fang, Zhaoyuan; Zhang, Jian; Li, Chen; Liu, Hongyan; Xia, Jufeng; Zhu, Hongwen; Guo, Chenchen; Qin, Zhen; Li, Fuming; Han, Xiuxin; Wang, Yuetong; Feng, Yan; Wang, Ye; Zhang, Wenjing; Wang, Zuoyun; Jin, Yujuan; Sun, Yihua; Wei, Wenyi; Zeng, Rong; Chen, Haiquan; Ji, Hongbin

doi:10.1038/cr.2016.111

Cited by 30 publications

(21 citation statements)

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“…Tra2β has been proven to be upregulated in various types of cancer including lung squamous cell carcinoma, glioma cancer, and prostate cancer . Tra2β is involved in several important processes including cell proliferation, epithelial‐to‐mesenchymal transition, invasion, and metastasis .…”

Section: Discussionmentioning

confidence: 99%

“…This raises the possibility that Tra2β may be a prognostic parameter for LSCC and provides the possibility of using Tra2β in individualization of both patient prognosis and therapy. Tra2β has been proven to be upregulated in various types of cancer including lung squamous cell carcinoma, 36 glioma cancer, 14 and prostate cancer. 15 Tra2β is involved in several important processes including cell proliferation, epithelial-to-mesenchymal transition, invasion, and metastasis.…”

Section: Discussionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…During the past few years, PEBP4 has been identified as a contributor to the development of numerous types of cancer (6)(7)(8)(9)20,21). Our previous study indicated that overexpression of PEBP4 enhances NSCLC cell proliferation and the invasive ability of cancer cells, while inhibiting apoptosis (9).…”

Section: Discussionmentioning

confidence: 99%

PEBP4 gene expression in lung squamous cell carcinoma: A meta‑analysis‑based study of the molecular pathways involved

Zhong

Huang

et al. 2020

Oncol Lett

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Previous studies have suggested increased activity of phosphatidylethanolamine binding protein 4 (PEBP4) may be associated with the prognosis of non-small cell lung cancer. However, to the best of our knowledge, no direct association between PEBP4 and lung squamous cell carcinoma (LSCC) has been reported. In the present study, a systematic review and meta-analysis was performed to examine the gene expression activity of PEBP4 in LSCC. A total of 10 out of 131 gene expression datasets from the Gene Expression Omnibus (GEO) were selected, including 574 samples (319 patients with LSCC and 255 healthy controls). Subsequently, multiple linear regression (MLR) was employed to study three potential influencing factors: Sample size, population region and study date. A literature-based pathway analysis was then conducted to examine the potential mechanisms through which PEBP4 may exert influence on LSCC. The results of a meta-analysis indicated that, in LSCC, PEBP4 exhibited significantly low expression levels (P<0.033), with mildly increased gene expression levels observed in three studies (log fold-change: 0.072-2.13). However, a significant between-study variance was observed from the heterogeneity analysis. MLR indicated that population region was a significant factor (P<0.0065), whereas sample size and study age were not (P>0.46). Eight functional pathways were subsequently identified, through which PEBP4 may influence the prognosis of LSCC and its response to treatment. The results of the present study suggested that the effects of PEBP4 on LSCC can be neglected in most cases of LSCC, where PEBP4 demonstrated decreased expression levels. However, in the case of PEBP4 overexpression, it may contribute to the progression of LSCC and lead to the development of drug resistance.

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“…For example, it has been reported that a single nucleotide polymorphism in dynein axonemal heavy chain (DNAH5) could be related to hyperinflation in COPD patients 91 . Other authors have described that the oncogenic driver originated by the association of DNAH5 and transformer-2 protein homolog beta (TRA2B) genes might have a role in the development of squamous cell lung cancer 92 .…”

Section: Several Potential Pathogenic Mechanisms Could Explain the LImentioning

confidence: 99%

Lung Hyperinflation in Chronic Obstructive Pulmonary Disease: Clinical and Therapeutic Relevance

García‐Río¹

2021

BRN

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Patients with chronic obstructive pulmonary disease (COPD) develop lung hyperinflation due to limited expiratory flow, loss of elastic recoil of the lungs or the combination of both, a circumstance that can become intensified during exercise. The increased operating lung volumes, both at rest and during exercise, overload the inspiratory muscles and limit the capacity for lung expansion, resulting in a neuro-mechanical uncoupling that generates or intensifies dyspnoea and limits exercise tolerance. In addition, lung hyperinflation can contribute to cardiovascular dysfunction during exercise and be a risk factor for the development of lung cancer. Bronchodilators are effective for reducing lung hyperinflation, both in static and dynamic situations, and other therapeutic alternatives are also available. In short, lung hyperinflation is a treatable trait of COPD with an important clinical and prognostic impact that requires specific attention.

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Identification of TRA2B-DNAH5 fusion as a novel oncogenic driver in human lung squamous cell carcinoma

Cited by 30 publications

References 50 publications

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

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

PEBP4 gene expression in lung squamous cell carcinoma: A meta‑analysis‑based study of the molecular pathways involved

Lung Hyperinflation in Chronic Obstructive Pulmonary Disease: Clinical and Therapeutic Relevance

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