Decreased expression of claudin-3 is associated with a poor prognosis and EMT in completely resected squamous cell lung carcinoma

Che, Juanjuan; Yang, Yifan; Xiao, Jing; Zhao, Pengfei; Yan, Bo; Dong, Shuang; Cao, Bangwei

doi:10.1007/s13277-015-3350-1

Cited by 23 publications

(24 citation statements)

References 37 publications

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“…Taken together, our results suggest that MAOA may play a role in promoting the progression of NSCLC. EMT, a key step in invasion and metastasis, plays a crucial role in the progression of cancers, including NSCLC (16)(17)(18)(19). Wu et al (25) demonstrated that MAOA expression in prostate cancer suppressed epithelial phenotype and promoted mesenchymal transition by decreasing the expression of epithelial marker E-cadherin, while increasing the expressions of mesenchymal marker vimentin and transcription factor Twist, indicating its association with EMT in prostate cancer.…”

Section: Discussionmentioning

confidence: 99%

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Increased expression of monoamine oxidase A is associated with epithelial to mesenchymal transition and clinicopathological features in non-small cell lung cancer

Liu

et al. 2017

Oncol Lett

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Abstract. Monoamine oxidase A (MAOA), a mitochondrial enzyme, is closely associated with neurological disorders. Recently, MAOA has been linked to the progression of prostate cancer, hepatocellular carcinoma, and cholangiocarcinoma. However, MAOA was reported to have different effects on the progression of these types of cancer, and the role of MAOA in non-small cell lung cancer (NSCLC) progression remains unclear. The present study determined the expression of MAOA and epithelial to mesenchymal transition (EMT) markers in 45 pairs of NSCLC and matched non-tumor adjacent lung tissues, and further analyzed the correlation between MAOA expression and the EMT or the development of clinicopathological features. The results demonstrated that protein and mRNA expression levels of MAOA in NSCLC tissues were higher than those observed in the matched non-tumor adjacent lung tissues. Furthermore, the increased MAOA expression in NSCLC tissues was positively correlated with N-cadherin (r=0.525, P=0.002), Slug (r=0.515, P=0.001), and Twist (r=0.448, P= 0.008) expressions, but negatively correlated with E-cadherin expression (r=-0.387, P=0.01). Additionally, the elevated MAOA expression in NSCLC tissues was associated with late stage NSCLC (Z=-2.596, P=0.029) and lymph node metastases (Z=-2.378, P= 0.020). These findings suggest that MAOA may have a role in promoting NSCLC progression by mediating EMT. IntroductionLung cancer, the leading cause of cancer-related deaths worldwide, is commonly divided into two categories, small cell lung cancer (SCLC) and non-SCLC (NSCLC), depending on its degree of differentiation and morphological characteristics (1,2). NSCLC accounts for ~80% of primary lung cancers, including squamous cell carcinoma, adenocarcinoma, and large cell carcinoma (3). The 5-year survival rate of NSCLC is only 7% (4). Moreover, lymph nodes and distant organ metastasis are the main reasons leading to treatment failure in NSCLC patients with radical resection (5,6).Epithelial to mesenchymal transition (EMT), a reversible biological process, is characterized by the loss of epithelial cell junction proteins (E-cadherin, Zo-1) (7,8), the gain of mesenchymal markers (vimentin, N-cadherin) (9,10), and the activation of transcription factors (Snail1, Slug, ZEB1, Twist) (11-15). Accumulating evidence indicates that EMT enhances tumor invasion, distant metastasis, and chemotherapy resistance in NSCLC, underscoring the need for a comprehensive understanding of the EMT function in NSCLC progression (16)(17)(18)(19).Monoamine oxidase A (MAOA), a mitochondria-bound enzyme, catalyzes the oxidative deamination of dietary amines and monoamine neurotransmitters, such as serotonin, norepinephrine, and dopamine (20,21). The functions of MAOA have been extensively studied in the context of neurological disorders, including mental depression, aggressive behaviors, and Parkinson's disease (22,23

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Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicates that EMT enhances tumor invasion, distant metastasis, and chemotherapy resistance in NSCLC, underscoring the need for a comprehensive understanding of the EMT function in NSCLC progression (16)(17)(18)(19).…”

Section: Introductionmentioning

confidence: 99%

Increased expression of monoamine oxidase A is associated with epithelial to mesenchymal transition and clinicopathological features in non-small cell lung cancer

Liu

et al. 2017

Oncol Lett

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“…In contrast, the ectopic expression of CLDN3 in hepatocellular carcinoma cells could inhibit tumorigenesis and cancerous cells migration and invasion [33]. A recent study revealed that downregulation of CLDN3 in SqCC patients is an independent prognostic factor for DFS, and correlated with an decreased expression of E-cadherin and β-catenin and an upregulation of vimentin [34]. However, compared to SqCC and normal tissue, an increased expression of CLDN3 was found in ADC [19–21].…”

Section: Discussionmentioning

confidence: 99%

Claudin-3 expression increases the malignant potential of lung adenocarcinoma cells: role of epidermal growth factor receptor activation

et al. 2017

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Claudins are essential for the formation and maintenance of tight junctions (TJ). The altered expression of claudin proteins has been described in a variety of malignancies. However, the alteration of these proteins in lung adenocarcinoma (ADC) are poorly understood. Therefore, we report, based on the protein expression analysis of a total of 275 patient samples, that claudin-3 (CLDN3) expression is significantly increased in ADC tissues and is associated with cancer progression, correlating significantly with the poor survival of ADC patients (p=0.041&0.029). More importantly, forcing CLDN3 expression in ADC cells without endogenous CLDN3 expression resulted in significant increases in the cell proliferation, anchorage-dependent growth, migration and drug-resistance. In addition, epidermal growth factor (EGF) signaling pathway modulates the expression of claudins in a number of solid tumors. However, the mechanism of tight junction regulation by EGF in ADC remains unclear. To investigate this mechanisms, ADC cell lines were treated with EGF and its inhibitor. EGF unregulated CLDN3 expression via the MEK/ERK or PI3K/Akt signaling pathways and was required for the maintenance of baseline CLDN3 expression. Furthermore, downregulation of CLDN3 expression in ADC cell was found to prevent the EGF-induced increase in cell proliferation. In conclusion, our results demonstrate a novel role of CLDN3 overexpression in promoting the malignant potential of lung adenocarcinoma. This function is potentially regulated by the EGF-activated MEK/ERK and PI3K-Akt pathways.

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“…In resected squamocellular lung cancers, reduced claudin 3 expression has been found to be associated with increased vimentin protein expression and also poor survival [15]. As far as we know, no previous data exists on claudin in relation to vimentin, Zeb1 and Sip1 expression in breast cancers.…”

Section: Discussionmentioning

confidence: 95%

“…Low-level claudin 4 expression is associated with poor prognosis in esophageal and pancreatic carcinoma [12,13]. On the other hand, claudin 3 overexpression is an indicator of poor prognosis in serous ovarian carcinoma, while its downregulation predicts poor survival in squamous cell lung carcinoma [14,15]. Low-level claudin 7 expression is associated with better prognosis of patients with oral squamous cell carcinoma [16], and in prostate carcinoma, with increased tumor grade [17].…”

Section: Introductionmentioning

confidence: 99%

High-level cytoplasmic claudin 3 expression is an independent predictor of poor survival in triple-negative breast cancer

et al. 2018

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Background: The subtype of claudin-low breast cancer can be reliably determined only by gene-expression profiling. Attempts have been made to develop immunohistochemical surrogates, which nearly always focus on membranous claudin expression. Methods: We assessed the immunohistochemical expression of both membranous and cytoplasmic claudins 3, 4 and 7 in a series of 197 non-metastatic breast cancers, enriched with triple-negative breast cancers (TNBCs; 60%). The expression of epithelial-to-mesenchymal transition-regulating transcription factors Sip1, Zeb1 and vimentin had previously been determined in the same material.

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Decreased expression of claudin-3 is associated with a poor prognosis and EMT in completely resected squamous cell lung carcinoma

Cited by 23 publications

References 37 publications

Increased expression of monoamine oxidase A is associated with epithelial to mesenchymal transition and clinicopathological features in non-small cell lung cancer

Increased expression of monoamine oxidase A is associated with epithelial to mesenchymal transition and clinicopathological features in non-small cell lung cancer

Claudin-3 expression increases the malignant potential of lung adenocarcinoma cells: role of epidermal growth factor receptor activation

High-level cytoplasmic claudin 3 expression is an independent predictor of poor survival in triple-negative breast cancer

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