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miR-195 is a key regulator of Raf1 in thyroid cancer.

Wang F, Jiang C, Sun Q, Yan F, Wang L, Fu Z, Liu T, Hu F - Onco Targets Ther (2015)

Bottom Line: Proto-oncogene Raf1 serves as a part of the mitogen-activated protein kinases/extracellular signal-regulated kinase signal transduction pathway and regulates cell migration, apoptosis, and differentiation.We also find that the expression of miR-195 is downregulated in 50 pairs of thyroid tumor tissues compared to the adjacent nontumor tissues, while there is no difference in the expression of miR-15a/b and miR-16 between the groups.Furthermore, exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology, Zhejiang Cancer Hospital, Zhejiang, Hangzhou, People's Republic of China ; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Zhejiang, Hangzhou, People's Republic of China.

ABSTRACT
Proto-oncogene Raf1 serves as a part of the mitogen-activated protein kinases/extracellular signal-regulated kinase signal transduction pathway and regulates cell migration, apoptosis, and differentiation. Although a large number of studies have shown that Raf1 is overexpressed in various kinds of cancer, little is known about the association between Raf1 and miRNAs in thyroid carcinoma. This study proves that Raf1 is overexpressed in thyroid cancer, which has been confirmed by many other studies. Besides, we identify that Raf1 is a direct target of miR-15a/b, miR-16, and miR-195 by dual luciferase reporter assay. We also find that the expression of miR-195 is downregulated in 50 pairs of thyroid tumor tissues compared to the adjacent nontumor tissues, while there is no difference in the expression of miR-15a/b and miR-16 between the groups. Furthermore, exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation. Our findings delineate a novel mechanism for the regulation of Raf1 in thyroid cancer, which may help to provide a new direction for the treatment of thyroid cancer.

No MeSH data available.


Related in: MedlinePlus

Overexpression of miR-195 inhibits cell proliferation.Notes: (A) Growth curve by counting cell number in B-CPAP overexpression stable cell lines. (B) Growth curve by counting cell number in ACT-1 overexpression stable cell lines. Cell amounts in each sample is measured daily in triplicates, and three independent experiments are performed. Data are expressed as mean ± SD.Abbreviations: SD, standard deviation; NC, negative control; LV, lentivirus.
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f6-ott-8-3021: Overexpression of miR-195 inhibits cell proliferation.Notes: (A) Growth curve by counting cell number in B-CPAP overexpression stable cell lines. (B) Growth curve by counting cell number in ACT-1 overexpression stable cell lines. Cell amounts in each sample is measured daily in triplicates, and three independent experiments are performed. Data are expressed as mean ± SD.Abbreviations: SD, standard deviation; NC, negative control; LV, lentivirus.

Mentions: Previous studies have suggested that Raf1 is involved in cellular proliferation, so we decide to determine whether overexpression of miR-195 could suppress the growth of thyroid cancer. The growth curve assays were conducted by counting the cell number. As expected, cellular proliferation is significantly impaired in miR-195 overexpressing thyroid cancer cells (Figure 6). These results indicate that miR-195 plays an important role in regulating the proliferation of thyroid cancer cells.


miR-195 is a key regulator of Raf1 in thyroid cancer.

Wang F, Jiang C, Sun Q, Yan F, Wang L, Fu Z, Liu T, Hu F - Onco Targets Ther (2015)

Overexpression of miR-195 inhibits cell proliferation.Notes: (A) Growth curve by counting cell number in B-CPAP overexpression stable cell lines. (B) Growth curve by counting cell number in ACT-1 overexpression stable cell lines. Cell amounts in each sample is measured daily in triplicates, and three independent experiments are performed. Data are expressed as mean ± SD.Abbreviations: SD, standard deviation; NC, negative control; LV, lentivirus.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4621222&req=5

f6-ott-8-3021: Overexpression of miR-195 inhibits cell proliferation.Notes: (A) Growth curve by counting cell number in B-CPAP overexpression stable cell lines. (B) Growth curve by counting cell number in ACT-1 overexpression stable cell lines. Cell amounts in each sample is measured daily in triplicates, and three independent experiments are performed. Data are expressed as mean ± SD.Abbreviations: SD, standard deviation; NC, negative control; LV, lentivirus.
Mentions: Previous studies have suggested that Raf1 is involved in cellular proliferation, so we decide to determine whether overexpression of miR-195 could suppress the growth of thyroid cancer. The growth curve assays were conducted by counting the cell number. As expected, cellular proliferation is significantly impaired in miR-195 overexpressing thyroid cancer cells (Figure 6). These results indicate that miR-195 plays an important role in regulating the proliferation of thyroid cancer cells.

Bottom Line: Proto-oncogene Raf1 serves as a part of the mitogen-activated protein kinases/extracellular signal-regulated kinase signal transduction pathway and regulates cell migration, apoptosis, and differentiation.We also find that the expression of miR-195 is downregulated in 50 pairs of thyroid tumor tissues compared to the adjacent nontumor tissues, while there is no difference in the expression of miR-15a/b and miR-16 between the groups.Furthermore, exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation.

View Article: PubMed Central - PubMed

Affiliation: Department of Radiation Oncology, Zhejiang Cancer Hospital, Zhejiang, Hangzhou, People's Republic of China ; Zhejiang Key Laboratory of Radiation Oncology, Zhejiang Cancer Hospital, Zhejiang, Hangzhou, People's Republic of China.

ABSTRACT
Proto-oncogene Raf1 serves as a part of the mitogen-activated protein kinases/extracellular signal-regulated kinase signal transduction pathway and regulates cell migration, apoptosis, and differentiation. Although a large number of studies have shown that Raf1 is overexpressed in various kinds of cancer, little is known about the association between Raf1 and miRNAs in thyroid carcinoma. This study proves that Raf1 is overexpressed in thyroid cancer, which has been confirmed by many other studies. Besides, we identify that Raf1 is a direct target of miR-15a/b, miR-16, and miR-195 by dual luciferase reporter assay. We also find that the expression of miR-195 is downregulated in 50 pairs of thyroid tumor tissues compared to the adjacent nontumor tissues, while there is no difference in the expression of miR-15a/b and miR-16 between the groups. Furthermore, exogenous overexpression of miR-195 significantly inhibits the protein expression of Raf1 and blocks the thyroid cancer cell proliferation. Our findings delineate a novel mechanism for the regulation of Raf1 in thyroid cancer, which may help to provide a new direction for the treatment of thyroid cancer.

No MeSH data available.


Related in: MedlinePlus