Cisplatin resistance in gastric cancer cells is associated with HER2 upregulation-induced epithelial-mesenchymal transition

Huang, Dongsheng; Duan, Hongying; Huang, Hao; Tong, Xiangmin; Han, Yong; Ru, Guoqing; Qu, Like; Shou, Chengchao; Zhao, Zhenze

doi:10.1038/srep20502

Cited by 85 publications

(62 citation statements)

References 53 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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“…DDP, a chemotherapy drug commonly used to treat gastric cancer [20–22] acts by inducing mitochondrial apoptosis in cancer cells; however, drug-resistant gastric cancer cells are not sensitive to this agent, and thus, considerable attention has been placed on this issue [23, 24]. Studies have indicated that TCM combination with chemotherapy for cancer can enhance the efficacy of and diminish the side effects and complications caused by chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

The Zuo Jin Wan Formula Induces Mitochondrial Apoptosis of Cisplatin-Resistant Gastric Cancer Cells via Cofilin-1

Tang

Sun

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Despite the status of cisplatin (DDP) as a classical chemotherapeutic agent in the treatment of cancer, the development of multidrug resistance often leads to a failure of DDP therapy. Here we found that phosphorylated cofilin-1 (p-cofilin-1) was overexpressed in the DDP-resistant human gastric cancer cell lines SGC7901/DDP and BGC823/DDP, relative to the respective parent cell lines (SGC7901 and BGC823), and that DDP induced the dephosphorylation of p-cofilin-1 in both parent lines but not in the DDP-resistant lines. However, we noted that the traditional Chinese medicine formula Zuo Jin Wan (ZJW) could induce the dephosphorylation of p-cofilin-1 and promote cofilin-1 translocation from the cytoplasm into the mitochondria in both SGC7901/DDP and BGC823/DDP cells. This mitochondrial translocation of cofilin-1 was found to induce the conversion of filamentous actin to globular-actin, activate mitochondrial damage and calcium overloading, and induce the mitochondrial apoptosis pathway. We further observed that these effects of ZJW on DDP-resistant human gastric cancer cell lines could be reversed via transfection with cofilin-1-specific siRNA, or treatment with a PP1 and PP2A inhibitor. These results suggest that ZJW is an effective drug therapy for patients with DDP-resistant gastric cancer.

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“…As the chemoresistant effects of RAS or PIK3CA pathway activation have already been described in several malignancies (7)(8)(9), they may apply to gastroesophageal cancer. HER2 positive patients appeared less likely to have TRG 1-2 in this study, but this requires further verification, as well (10). Therefore, the above findings must be interpreted with caution, as resection specimens were already molecularly and biologically modified by preoperative chemotherapy.…”

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confidence: 90%

Pathologic tumor response to neoadjuvant chemotherapy in gastroesophageal cancer: what does it mean?

Kosuga¹,

Ichikawa²,

Otsuji³

2016

Transl. Gastroenterol. Hepatol.

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Cisplatin resistance in gastric cancer cells is associated with HER2 upregulation-induced epithelial-mesenchymal transition

Cited by 85 publications

References 53 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

The Zuo Jin Wan Formula Induces Mitochondrial Apoptosis of Cisplatin-Resistant Gastric Cancer Cells via Cofilin-1

Pathologic tumor response to neoadjuvant chemotherapy in gastroesophageal cancer: what does it mean?

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