Limits...
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 cell migration and invasion in vitro. a Cell migratory ability detected by wound healing assay. b Cell migratory ability detected by Transwell migration assay. c Cell invasive ability detected by Transwell invasion assay. 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
getmorefigures.php?uid=PMC4621856&req=5

Fig3: MiR-24 inhibits NPC cell migration and invasion in vitro. a Cell migratory ability detected by wound healing assay. b Cell migratory ability detected by Transwell migration assay. c Cell invasive ability detected by Transwell invasion assay. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test

Mentions: We further evaluated the effect of miR-24 on the migratory and invasive ability of NPC cells after transient transfection with miR-24 mimics or miR controls. The wound healing assay showed that the migratory ability of SUNE-1 and CNE-2 cells transfected with miR-24 mimics was much weaker than those transfected with miR controls (Fig. 3a). Transwell migration assay also demonstrated that overexpression of miR-24 remarkably suppressed the migratory ability of NPC cells (Fig. 3b, P < 0.05). In addition, Transwell invasion assay indicated that the invasive ability was inhibited by transfecting with miR-24 mimics (Fig. 3c, P < 0.05).Fig. 3


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 cell migration and invasion in vitro. a Cell migratory ability detected by wound healing assay. b Cell migratory ability detected by Transwell migration assay. c Cell invasive ability detected by Transwell invasion assay. 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

Fig3: MiR-24 inhibits NPC cell migration and invasion in vitro. a Cell migratory ability detected by wound healing assay. b Cell migratory ability detected by Transwell migration assay. c Cell invasive ability detected by Transwell invasion assay. Data is presented as the mean ± SD; P values were calculated with the Student’s t-test
Mentions: We further evaluated the effect of miR-24 on the migratory and invasive ability of NPC cells after transient transfection with miR-24 mimics or miR controls. The wound healing assay showed that the migratory ability of SUNE-1 and CNE-2 cells transfected with miR-24 mimics was much weaker than those transfected with miR controls (Fig. 3a). Transwell migration assay also demonstrated that overexpression of miR-24 remarkably suppressed the migratory ability of NPC cells (Fig. 3b, P < 0.05). In addition, Transwell invasion assay indicated that the invasive ability was inhibited by transfecting with miR-24 mimics (Fig. 3c, P < 0.05).Fig. 3

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