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Small nucleolar RNA 78 promotes the tumorigenesis in non-small cell lung cancer.

Zheng D, Zhang J, Ni J, Luo J, Wang J, Tang L, Zhang L, Wang L, Xu J, Su B, Chen G - J. Exp. Clin. Cancer Res. (2015)

Bottom Line: A great upregulation of SNORD78 was observed in cancer tissues compared to their adjacent normal tissues.Meanwhile, patients with high SNORD78 expression have significantly poorer prognosis than those with low expression.The oncogenic activity of SNORD78 was also confirmed with in vivo data.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Zhengmin Road, Shanghai, 200433, People's Republic of China. zhengdiok@aliyun.com.

ABSTRACT

Background: Accumulating evidence suggests that dysregulated snoRNA may play a role in the development of malignancy. In the present study, we investigated the role of SNORD78 in the tumorigenesis of non-small cell lung cancer (NSCLC).

Methods: We determined the expression level of SNORD78 in NSCLC tissues with quantitative real-time PCR and then studied its clinical significance. We explored the biological significance of SNORD78 with gain-and-loss-of-function analyses both in vitro and in vivo.

Results: A great upregulation of SNORD78 was observed in cancer tissues compared to their adjacent normal tissues. Meanwhile, patients with high SNORD78 expression have significantly poorer prognosis than those with low expression. Inhibition of SNORD78 suppressed the proliferation of NSCLC cells via inducing G0/G1 cell cycle arrest and apoptosis while SNORD78 overexpression promoted the cell proliferation. SNORD78 promoted invasion of NSCLC cells via inducing epithelial-mesenchymal-transition (EMT). SNORD78 was also obviously upregulated in cancer stem-like cells and is required for the self-renewal of NSCLC. The oncogenic activity of SNORD78 was also confirmed with in vivo data.

Conclusion: Our study identified that SNORD78 may be a potential therapeutic target for NSCLC.

No MeSH data available.


Related in: MedlinePlus

The effects of SNORD78 on in vivo tumor growth of NSCLC. Inhibition of SNORD78 suppressed tumor growth in subcutaneous implantation mouse models of H1975 cells. Tumor growth curves (a) and tumor volumes (b) of subcutaneous implantation models of gallbladder cancer are shown. (c) H&E and immunohistochemical staining demonstrated that suppression of SNORD78 inhibited the aggressive phenotype of NSCLC cells in vivo, as indicated by the expression of Ki67-positive and caspase-3-positive cells. *, p < 0.05; **, p < 0.01
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Fig7: The effects of SNORD78 on in vivo tumor growth of NSCLC. Inhibition of SNORD78 suppressed tumor growth in subcutaneous implantation mouse models of H1975 cells. Tumor growth curves (a) and tumor volumes (b) of subcutaneous implantation models of gallbladder cancer are shown. (c) H&E and immunohistochemical staining demonstrated that suppression of SNORD78 inhibited the aggressive phenotype of NSCLC cells in vivo, as indicated by the expression of Ki67-positive and caspase-3-positive cells. *, p < 0.05; **, p < 0.01

Mentions: To validate the effect of SNORD78 on NSCLC cell tumorigenesis in vivo, H1975-shRNA-SNORD78 or H1975-shRNA-control cells were injected into flanks of nude mice. Palpable tumors formed with 1 week. Tumor volume was measured on a weekly basis. Four weeks after injection, the average tumor volume of H1975 cells transfected with shRNA-SNORD78 was 1.35 ± 0.34 cm3, which was significantly lower than tumors in the control group (2.51 ± 0.48 cm3, p < 0.01; Fig. 7a,b). Immunohistochemical staining of tumor tissues indicated a decrease in ki67 and an increase in cleaved caspase-3 in shRNA-SNORD78 vs. shRNA-control (Fig. 7c). The in vivo data complement the in vitro studies of SNORD78 and confirm the oncogenic activity of SNORD78 in NSCLC.Fig. 7


Small nucleolar RNA 78 promotes the tumorigenesis in non-small cell lung cancer.

Zheng D, Zhang J, Ni J, Luo J, Wang J, Tang L, Zhang L, Wang L, Xu J, Su B, Chen G - J. Exp. Clin. Cancer Res. (2015)

The effects of SNORD78 on in vivo tumor growth of NSCLC. Inhibition of SNORD78 suppressed tumor growth in subcutaneous implantation mouse models of H1975 cells. Tumor growth curves (a) and tumor volumes (b) of subcutaneous implantation models of gallbladder cancer are shown. (c) H&E and immunohistochemical staining demonstrated that suppression of SNORD78 inhibited the aggressive phenotype of NSCLC cells in vivo, as indicated by the expression of Ki67-positive and caspase-3-positive cells. *, p < 0.05; **, p < 0.01
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4472183&req=5

Fig7: The effects of SNORD78 on in vivo tumor growth of NSCLC. Inhibition of SNORD78 suppressed tumor growth in subcutaneous implantation mouse models of H1975 cells. Tumor growth curves (a) and tumor volumes (b) of subcutaneous implantation models of gallbladder cancer are shown. (c) H&E and immunohistochemical staining demonstrated that suppression of SNORD78 inhibited the aggressive phenotype of NSCLC cells in vivo, as indicated by the expression of Ki67-positive and caspase-3-positive cells. *, p < 0.05; **, p < 0.01
Mentions: To validate the effect of SNORD78 on NSCLC cell tumorigenesis in vivo, H1975-shRNA-SNORD78 or H1975-shRNA-control cells were injected into flanks of nude mice. Palpable tumors formed with 1 week. Tumor volume was measured on a weekly basis. Four weeks after injection, the average tumor volume of H1975 cells transfected with shRNA-SNORD78 was 1.35 ± 0.34 cm3, which was significantly lower than tumors in the control group (2.51 ± 0.48 cm3, p < 0.01; Fig. 7a,b). Immunohistochemical staining of tumor tissues indicated a decrease in ki67 and an increase in cleaved caspase-3 in shRNA-SNORD78 vs. shRNA-control (Fig. 7c). The in vivo data complement the in vitro studies of SNORD78 and confirm the oncogenic activity of SNORD78 in NSCLC.Fig. 7

Bottom Line: A great upregulation of SNORD78 was observed in cancer tissues compared to their adjacent normal tissues.Meanwhile, patients with high SNORD78 expression have significantly poorer prognosis than those with low expression.The oncogenic activity of SNORD78 was also confirmed with in vivo data.

View Article: PubMed Central - PubMed

Affiliation: Department of Medical Oncology, Shanghai Pulmonary Hospital, Tongji University School of Medicine, 507 Zhengmin Road, Shanghai, 200433, People's Republic of China. zhengdiok@aliyun.com.

ABSTRACT

Background: Accumulating evidence suggests that dysregulated snoRNA may play a role in the development of malignancy. In the present study, we investigated the role of SNORD78 in the tumorigenesis of non-small cell lung cancer (NSCLC).

Methods: We determined the expression level of SNORD78 in NSCLC tissues with quantitative real-time PCR and then studied its clinical significance. We explored the biological significance of SNORD78 with gain-and-loss-of-function analyses both in vitro and in vivo.

Results: A great upregulation of SNORD78 was observed in cancer tissues compared to their adjacent normal tissues. Meanwhile, patients with high SNORD78 expression have significantly poorer prognosis than those with low expression. Inhibition of SNORD78 suppressed the proliferation of NSCLC cells via inducing G0/G1 cell cycle arrest and apoptosis while SNORD78 overexpression promoted the cell proliferation. SNORD78 promoted invasion of NSCLC cells via inducing epithelial-mesenchymal-transition (EMT). SNORD78 was also obviously upregulated in cancer stem-like cells and is required for the self-renewal of NSCLC. The oncogenic activity of SNORD78 was also confirmed with in vivo data.

Conclusion: Our study identified that SNORD78 may be a potential therapeutic target for NSCLC.

No MeSH data available.


Related in: MedlinePlus