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MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1.

Li YQ, Lu JH, Bao XM, Wang XF, Wu JH, Hong WQ - J. Exp. Clin. Cancer Res. (2015)

Bottom Line: The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05).Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05).Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target.

View Article: PubMed Central - PubMed

Affiliation: Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China. hare0914@gzhmu.edu.cn.

ABSTRACT

Background: Increasing evidence indicates that the dysregulation of miRNAs expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. However, no study investigates the function and mechanisms of miR-24 in nasopharyngeal carcinoma (NPC).

Methods: Quantitative RT-PCR, MTT, colony formation, soft-agar, wound healing, Transwell migration and invasion assays, and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of miR-24 in NPC. Luciferase reporter assay, quantitative RT-PCR, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-24.

Results: The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05). Ectopic expression of miR-24 inhibited the cell viability, proliferation, migration, and invasion in vitro (all P < 0.05), and suppressed the xenograft tumor growth and lung metastasis formation in vivo (all P < 0.05). Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05).

Conclusions: Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target.

No MeSH data available.


Related in: MedlinePlus

MiR-24 inhibits NPC xenograft tumor growth and lung metastasis in vivo. a Representative images of tumors formed and the growth curves of tumor volume. b Representative images of tumors formed and the tumor weight. c Representative images and quantification of macroscopic lung metastasis. d Representative images and quantification of microscopic lung metastatic nodes based on H&E staining. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test
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Fig4: MiR-24 inhibits NPC xenograft tumor growth and lung metastasis in vivo. a Representative images of tumors formed and the growth curves of tumor volume. b Representative images of tumors formed and the tumor weight. c Representative images and quantification of macroscopic lung metastasis. d Representative images and quantification of microscopic lung metastatic nodes based on H&E staining. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test

Mentions: Given that miR-24 inhibited the proliferation and invasion of NPC cells in vitro, we tested whether ectopic expression of miR-24 could affect the tumorigenesis and metastasis in vivo. Xenograft tumor growth and lung metastasis models were obtained as described in the methods section. As shown in Fig. 4a, tumors grew at a slower rate and had smaller volumes in the miR-24 overexpressing group than the control group (P < 0.05). The average tumor weight in the miR-24 overexpressing group was also significantly lower (0.27 ± 0.14 g vs. 0.67 ± 0.20 g; Fig. 4b, P < 0.05). In addition, fewer metastatic nodes were formed on the surface of lungs in the miR-24 overexpressing group than the control group (Fig. 4c, P < 0.05), which was further confirmed by H&E staining (Fig. 4d, P < 0.05).Fig. 4


MiR-24 functions as a tumor suppressor in nasopharyngeal carcinoma through targeting FSCN1.

Li YQ, Lu JH, Bao XM, Wang XF, Wu JH, Hong WQ - J. Exp. Clin. Cancer Res. (2015)

MiR-24 inhibits NPC xenograft tumor growth and lung metastasis in vivo. a Representative images of tumors formed and the growth curves of tumor volume. b Representative images of tumors formed and the tumor weight. c Representative images and quantification of macroscopic lung metastasis. d Representative images and quantification of microscopic lung metastatic nodes based on H&E staining. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4621856&req=5

Fig4: MiR-24 inhibits NPC xenograft tumor growth and lung metastasis in vivo. a Representative images of tumors formed and the growth curves of tumor volume. b Representative images of tumors formed and the tumor weight. c Representative images and quantification of macroscopic lung metastasis. d Representative images and quantification of microscopic lung metastatic nodes based on H&E staining. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test
Mentions: Given that miR-24 inhibited the proliferation and invasion of NPC cells in vitro, we tested whether ectopic expression of miR-24 could affect the tumorigenesis and metastasis in vivo. Xenograft tumor growth and lung metastasis models were obtained as described in the methods section. As shown in Fig. 4a, tumors grew at a slower rate and had smaller volumes in the miR-24 overexpressing group than the control group (P < 0.05). The average tumor weight in the miR-24 overexpressing group was also significantly lower (0.27 ± 0.14 g vs. 0.67 ± 0.20 g; Fig. 4b, P < 0.05). In addition, fewer metastatic nodes were formed on the surface of lungs in the miR-24 overexpressing group than the control group (Fig. 4c, P < 0.05), which was further confirmed by H&E staining (Fig. 4d, P < 0.05).Fig. 4

Bottom Line: The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05).Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05).Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target.

View Article: PubMed Central - PubMed

Affiliation: Guangzhou First People's hospital, Guangzhou Medical University, 1 Panfu Road, Guangzhou, Guangdong, 510180, PR China. hare0914@gzhmu.edu.cn.

ABSTRACT

Background: Increasing evidence indicates that the dysregulation of miRNAs expression is involved in the tumorigenesis by acting as tumor suppressors or oncogenes. However, no study investigates the function and mechanisms of miR-24 in nasopharyngeal carcinoma (NPC).

Methods: Quantitative RT-PCR, MTT, colony formation, soft-agar, wound healing, Transwell migration and invasion assays, and xenograft tumor growth and lung metastasis models were performed to test the expression levels and functions of miR-24 in NPC. Luciferase reporter assay, quantitative RT-PCR, Western blotting, and immunohistochemistry were used to identify and verify the target of miR-24.

Results: The results showed that MiR-24 was obviously downregulated in NPC cell lines and tissue samples (P < 0.05). Ectopic expression of miR-24 inhibited the cell viability, proliferation, migration, and invasion in vitro (all P < 0.05), and suppressed the xenograft tumor growth and lung metastasis formation in vivo (all P < 0.05). Fascin homologue 1 (FSCN1) was verified as a direct target of miR-24, and silencing FSCN1 expression with small interfering RNA inhibited NPC cell proliferation and invasion (all P < 0.05).

Conclusions: Overall, miR-24 acts as a novel tumor suppressor in the development and progression of NPC through targeting FSCN1, which providing new insight into the mechanisms of NPC carcinogenesis and suggesting the possibility of miR-24 as a therapeutic target.

No MeSH data available.


Related in: MedlinePlus