A directly negative interaction of miR-203 and ZEB2 modulates tumor stemness and chemotherapy resistance in nasopharyngeal carcinoma

Jiang, Qingping; Zhou, Ying; Yang, Huiling; Li, Libo; Deng, Xiaojie; Chen, Cheng; Xie, Yingying; Luo, Xiaojun; Fang, Weiyi; Liu, Zhen

doi:10.18632/oncotarget.11691

Cited by 34 publications

(33 citation statements)

References 41 publications

(42 reference statements)

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“…Jiang et al . demonstrate a direct negative feedback loop between miR‐203 and ZEB2 participating in tumor stemness and chemotherapy resistance of nasopharyngeal carcinoma . Zhang et al .…”

Section: Discussionmentioning

confidence: 59%

“…Jiang et al demonstrate a direct negative feedback loop between miR-203 and ZEB2 participating in tumor stemness and chemotherapy resistance of nasopharyngeal carcinoma. (25) Zhang et al report that miR-203 was epigenetically silenced, and the silencing promoted tumor cell growth and invasion at least in part by upregulating the Snai2 transcription factor in malignant breast cancer cells. (27) In this study, hepatectomy downregulated expression of E-cadherin and upregulated expression of vimentin and N-cadherin, whereas miR-203 overexpression upregulated E-cadherin expression and downregulated expressions of vimentin and Ncadherin.…”

Section: Discussionmentioning

confidence: 99%

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miR‐203 inhibits augmented proliferation and metastasis of hepatocellular carcinoma residual in the promoted regenerating liver

Zheng

Chen

et al. 2017

Cancer Science

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Liver resection is still the most commonly used therapeutic treatment for hepatocellular carcinoma (HCC), and liver regeneration promotes HCC growth in the regenerating liver. The high recurrence/metastasis of HCC is the main cause of death for HCC patients after liver resection. However, how the augmented growth and metastasis of residual HCC induced by the promoted liver regeneration following liver resection can be abolished remains unclear. In this study, a rat model with liver cirrhosis and diffused HCC was established by administration of diethylnitrosamine. Recombinant miR‐203 adenovirus was administered to induce hepatic miR‐203 overexpression and 30% partial hepatectomy (PH) followed. The effect of miR‐203 on the proliferation, invasion and metastasis of the residual HCC in the remnant cirrhotic liver with promoted regeneration was investigated. We found that the basic spontaneous regeneration of the non‐tumorous liver by 30% PH promoted proliferation, invasion and lung metastasis of the hepatic residual HCC. miR‐203 overexpression further promoted the regeneration of the non‐tumorous liver by upregulating Ki67 expression and enhancing IL‐6/SOCS3/STAT3 pro‐proliferative signals. Importantly, miR‐203 overexpression markedly inhibited the proliferation, invasion and metastasis of hepatic residual HCC through suppressing expression of Ki67, CAPNS1 and lung metastasis. Moreover, it was found that miR‐203 overexpression reversed the epithelial–mesenchymal transition induced by hepatectomy through targeting IL‐1β, Snail1 and Twist1. In conclusion, our results suggested that miR‐203 overexpression inhibited the augmented proliferation and lung metastasis of the residual HCC induced by the promoted liver regeneration following PH partly by regulating epithelial–mesenchymal transition.

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Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 99%

miR‐203 inhibits augmented proliferation and metastasis of hepatocellular carcinoma residual in the promoted regenerating liver

Zheng

Chen

et al. 2017

Cancer Science

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“…Wang, et al found that c-MYB strengthens the stemness of NPC cancer stem cell via down-regulating miR-143, thereby increasing the resistance to radiotherapy [86]. Other articles also mentioned the effects of miRNAs on the stemness of nasopharyngeal carcinoma cells and the regulation of apoptosis and damage repair of cells by affecting stemness [87].…”

Section: Mirnas Participate In Radiotherapy Resistance Of Nasopharyngmentioning

confidence: 99%

MiRNAs in Radiotherapy Resistance of Nasopharyngeal Carcinoma

Tian¹,

Tang²,

Yi³

et al. 2020

J. Cancer

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Nasopharyngeal carcinoma (NPC) is one of the most common malignant tumors of the head and neck in Southeast Asia and southern China. Although the comprehensive treatment based on intensity-modulated radiation therapy improves outcomes, the five-year survival rate of NPC patients is low, and the recurrence remains high. Radiotherapy resistance is the main cause of poor prognosis in NPC patients. MicroRNAs (miRNAs) are a class of endogenous non-coding RNAs regulating various biological functions in eukaryotes. These miRNAs can regulate the development and progression of nasopharyngeal carcinoma by affecting the proliferation, apoptosis, movement, invasion and metastasis of NPC cells. The abnormal expression of miRNAs is closely related to radiotherapy sensitivity and prognosis of NPC patients, which can affect the transmission of related signaling pathways by regulating the expression of tumor suppressor genes and / or oncogenes, and therefore participate in radiotherapy resistance in nasopharyngeal carcinoma. Here, we review the mechanisms by which miRNAs may be involved in the radiotherapy resistance of nasopharyngeal carcinoma.

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“…For instance, miR-203 has been documented to suppress NPC cell migration, invasion, tumor stemness, and chemotherapy resistance to DDP in vitro and in vivo, by targeting ZEB2 and downstream EMT and tumor stemness signals. 19 The miR-10b is upregulated in HNE1/DDP cells, and inhibition of miR-10b expression reversed the EMT phenotype. 20 Multiple molecules and various signaling pathways are involved in chemoresistance in human malignancies.…”

Section: Introductionmentioning

confidence: 98%

NEDD4 is involved in acquisition of epithelial-mesenchymal transition in cisplatin-resistant nasopharyngeal carcinoma cells

Feng

Yang

et al. 2017

Cell Cycle

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Nasopharyngeal carcinoma (NPC) is a highly invasive head-neck cancer derived from the nasopharyngeal epithelium, mainly prevalent in southern China and Southeast Asia. Radiotherapy and adjuvant cisplatin (DDP) chemotherapy are standard administrations applied in the treatment of NPC. However, resistance to chemotherapeutic drugs has recently become more common, resulting in worse treatment outcome for NPC therapy. To elucidate the underlying molecular basis of drug resistance to DDP in NPC cells, we examined the morphocytology, cell motility and molecular changes in DDP-resistant NPC cells with respect to epithelial-mesenchymal transition (EMT) features. We found that EMT is closely associated with DDP-induced drug resistance in NPC cells, as DDP-resistant cells displayed morphological and molecular markers changes consistent with EMT. Wound healing and Transwell Boyden chamber assays revealed an enhanced migration and invasion potential in DDP-resistant NPC cells. Mechanistically, upregulation of NEDD4 was observed to relate to EMT in DDP-resistant cells. More importantly, depletion of NEDD4 in resistant cells led to a partial reversion of EMT phenotypes to MET characteristics. These data suggest that NEDD4 is largely involved in EMT features and chemoresistance of NPC cancer cells. NEDD4 could be a novel therapeutic target to overcome drug resistance in successful administrations of NPC.

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A directly negative interaction of miR-203 and ZEB2 modulates tumor stemness and chemotherapy resistance in nasopharyngeal carcinoma

Cited by 34 publications

References 41 publications

miR‐203 inhibits augmented proliferation and metastasis of hepatocellular carcinoma residual in the promoted regenerating liver

miR‐203 inhibits augmented proliferation and metastasis of hepatocellular carcinoma residual in the promoted regenerating liver

MiRNAs in Radiotherapy Resistance of Nasopharyngeal Carcinoma

NEDD4 is involved in acquisition of epithelial-mesenchymal transition in cisplatin-resistant nasopharyngeal carcinoma cells

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