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MicroRNA‑205 promotes the tumorigenesis of nasopharyngeal carcinoma through targeting tumor protein p53-inducible nuclear protein 1.

Nie G, Duan H, Li X, Yu Z, Luo L, Lu R, Ji Z, Zhang W - Mol Med Rep (2015)

Bottom Line: The present study aimed to explore the potential role of miR‑205 in NPC.The expression of miR‑205 was increased in NPC tissues compared with that in normal tissues.Overexpression of miR‑205 was found to promote the proliferation, migration and invasion of NPC‑derived cells, while apoptosis was suppressed.

View Article: PubMed Central - PubMed

Affiliation: Department of Otolaryngology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, P.R. China.

ABSTRACT
Nasopharyngeal carcinoma (NPC) is a common type of cancer in southern China, miRNAs have been shown to be involved in the tumorigenesis of multiple cancer types. The present study aimed to explore the potential role of miR‑205 in NPC. Reverse transcription quantitative polymerase chain reaction was used to determine the expression levels of miR‑205 in 20 fresh NPC specimens and 20 normal nasopharyngeal tissues. The function of miR‑205 in the proliferation, migration, invasion and apoptosis of NPC‑derived cells was detected by MTT assay, colony formation assay, wound healing assay, Transwell assay and flow cytometry. Furthermore, a target gene of miR‑205 was identified using the luciferase reporter assay. The expression of miR‑205 was increased in NPC tissues compared with that in normal tissues. Overexpression of miR‑205 was found to promote the proliferation, migration and invasion of NPC‑derived cells, while apoptosis was suppressed. Tumor protein p53-inducible nuclear protein 1 was identified as a target gene of miR‑205. Overall, the present study demonstrated that miR‑205 may function as an oncogene in NPC tumorigenesis.

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Related in: MedlinePlus

Expression of miR-205 in 20 NPC tissues. Reverse transcription quantitative polymerase chain reaction analysis showed that miR-205 was upregulated in NPC tissues compared with that in normal nasopharyngeal tissues (P=0.002). Each data-point resembles the result for one patient, horizontal lines represent their mean value and error bars represent the standard deviation. *P<0.05. miR, microRNA; NPC, nasopharyngeal carcinoma.
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f1-mmr-12-04-5715: Expression of miR-205 in 20 NPC tissues. Reverse transcription quantitative polymerase chain reaction analysis showed that miR-205 was upregulated in NPC tissues compared with that in normal nasopharyngeal tissues (P=0.002). Each data-point resembles the result for one patient, horizontal lines represent their mean value and error bars represent the standard deviation. *P<0.05. miR, microRNA; NPC, nasopharyngeal carcinoma.

Mentions: As shown in Fig. 1, the expression of miR-205 was significantly upregulated in NPC tissues compared with that in the normal nasopharyngeal epithelial tissues, suggesting that overexpression of miR-205 may be important in NPC development and metastasis.


MicroRNA‑205 promotes the tumorigenesis of nasopharyngeal carcinoma through targeting tumor protein p53-inducible nuclear protein 1.

Nie G, Duan H, Li X, Yu Z, Luo L, Lu R, Ji Z, Zhang W - Mol Med Rep (2015)

Expression of miR-205 in 20 NPC tissues. Reverse transcription quantitative polymerase chain reaction analysis showed that miR-205 was upregulated in NPC tissues compared with that in normal nasopharyngeal tissues (P=0.002). Each data-point resembles the result for one patient, horizontal lines represent their mean value and error bars represent the standard deviation. *P<0.05. miR, microRNA; NPC, nasopharyngeal carcinoma.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581759&req=5

f1-mmr-12-04-5715: Expression of miR-205 in 20 NPC tissues. Reverse transcription quantitative polymerase chain reaction analysis showed that miR-205 was upregulated in NPC tissues compared with that in normal nasopharyngeal tissues (P=0.002). Each data-point resembles the result for one patient, horizontal lines represent their mean value and error bars represent the standard deviation. *P<0.05. miR, microRNA; NPC, nasopharyngeal carcinoma.
Mentions: As shown in Fig. 1, the expression of miR-205 was significantly upregulated in NPC tissues compared with that in the normal nasopharyngeal epithelial tissues, suggesting that overexpression of miR-205 may be important in NPC development and metastasis.

Bottom Line: The present study aimed to explore the potential role of miR‑205 in NPC.The expression of miR‑205 was increased in NPC tissues compared with that in normal tissues.Overexpression of miR‑205 was found to promote the proliferation, migration and invasion of NPC‑derived cells, while apoptosis was suppressed.

View Article: PubMed Central - PubMed

Affiliation: Department of Otolaryngology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, P.R. China.

ABSTRACT
Nasopharyngeal carcinoma (NPC) is a common type of cancer in southern China, miRNAs have been shown to be involved in the tumorigenesis of multiple cancer types. The present study aimed to explore the potential role of miR‑205 in NPC. Reverse transcription quantitative polymerase chain reaction was used to determine the expression levels of miR‑205 in 20 fresh NPC specimens and 20 normal nasopharyngeal tissues. The function of miR‑205 in the proliferation, migration, invasion and apoptosis of NPC‑derived cells was detected by MTT assay, colony formation assay, wound healing assay, Transwell assay and flow cytometry. Furthermore, a target gene of miR‑205 was identified using the luciferase reporter assay. The expression of miR‑205 was increased in NPC tissues compared with that in normal tissues. Overexpression of miR‑205 was found to promote the proliferation, migration and invasion of NPC‑derived cells, while apoptosis was suppressed. Tumor protein p53-inducible nuclear protein 1 was identified as a target gene of miR‑205. Overall, the present study demonstrated that miR‑205 may function as an oncogene in NPC tumorigenesis.

Show MeSH
Related in: MedlinePlus