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miR-211 suppresses hepatocellular carcinoma by downregulating SATB2.

Jiang G, Cui Y, Yu X, Wu Z, Ding G, Cao L - Oncotarget (2015)

Bottom Line: Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues.We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells.This study provides insights into molecular mechanisms that miR-211 contributed to HCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatopancreatobiliary Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

ABSTRACT
Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC.

No MeSH data available.


Related in: MedlinePlus

miR-211 repressed the growth of HepG2-engrafted tumors(A) Representative tumors were photographed at 15 days after the first treatment with miR-211 mimic or scramble. (B) Tumor weight averages between scrambled and miR-211 mimics-treated mice groups at the end of the experiment (day 25). (C) Graph representing tumor volumes at the indicated days during the experiment for the two groups: scrambled mimics, miR-211 mimics. (D) Injection of miR-211 reduced Ki-67 protein expression in HepG2 xenograft tumors. (E) Injection of miR-211 reduced STAB2 protein levels in HepG2 xenograft tumors. Represented are 2 tumors from each group. ***p < 0.001.
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Figure 7: miR-211 repressed the growth of HepG2-engrafted tumors(A) Representative tumors were photographed at 15 days after the first treatment with miR-211 mimic or scramble. (B) Tumor weight averages between scrambled and miR-211 mimics-treated mice groups at the end of the experiment (day 25). (C) Graph representing tumor volumes at the indicated days during the experiment for the two groups: scrambled mimics, miR-211 mimics. (D) Injection of miR-211 reduced Ki-67 protein expression in HepG2 xenograft tumors. (E) Injection of miR-211 reduced STAB2 protein levels in HepG2 xenograft tumors. Represented are 2 tumors from each group. ***p < 0.001.

Mentions: MiR-211 mimic injection repressed the growth of HepG2-engrafted tumors compared to scrambled oligonucleotides-treated tumors (Figure 7A). In agreement with the tumor growth curve, the volumes and weights of tumors treated by miR-211 mimics were also lower than scrambled mimics-treated tumors (Figure 7B and 7C). Western blot analysis in randomly selected xenograft mouse tumors showed that miR-211 mimics-injecting tumors expressed lower levels of STAB2 than scramble controls (Figure 7E). Moreover, Ki-67 was lower in the miR-211 mimics-injecting tumors compared to the scrambled mimics-treated tumors (Figure 7D).


miR-211 suppresses hepatocellular carcinoma by downregulating SATB2.

Jiang G, Cui Y, Yu X, Wu Z, Ding G, Cao L - Oncotarget (2015)

miR-211 repressed the growth of HepG2-engrafted tumors(A) Representative tumors were photographed at 15 days after the first treatment with miR-211 mimic or scramble. (B) Tumor weight averages between scrambled and miR-211 mimics-treated mice groups at the end of the experiment (day 25). (C) Graph representing tumor volumes at the indicated days during the experiment for the two groups: scrambled mimics, miR-211 mimics. (D) Injection of miR-211 reduced Ki-67 protein expression in HepG2 xenograft tumors. (E) Injection of miR-211 reduced STAB2 protein levels in HepG2 xenograft tumors. Represented are 2 tumors from each group. ***p < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4496230&req=5

Figure 7: miR-211 repressed the growth of HepG2-engrafted tumors(A) Representative tumors were photographed at 15 days after the first treatment with miR-211 mimic or scramble. (B) Tumor weight averages between scrambled and miR-211 mimics-treated mice groups at the end of the experiment (day 25). (C) Graph representing tumor volumes at the indicated days during the experiment for the two groups: scrambled mimics, miR-211 mimics. (D) Injection of miR-211 reduced Ki-67 protein expression in HepG2 xenograft tumors. (E) Injection of miR-211 reduced STAB2 protein levels in HepG2 xenograft tumors. Represented are 2 tumors from each group. ***p < 0.001.
Mentions: MiR-211 mimic injection repressed the growth of HepG2-engrafted tumors compared to scrambled oligonucleotides-treated tumors (Figure 7A). In agreement with the tumor growth curve, the volumes and weights of tumors treated by miR-211 mimics were also lower than scrambled mimics-treated tumors (Figure 7B and 7C). Western blot analysis in randomly selected xenograft mouse tumors showed that miR-211 mimics-injecting tumors expressed lower levels of STAB2 than scramble controls (Figure 7E). Moreover, Ki-67 was lower in the miR-211 mimics-injecting tumors compared to the scrambled mimics-treated tumors (Figure 7D).

Bottom Line: Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues.We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells.This study provides insights into molecular mechanisms that miR-211 contributed to HCC.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatopancreatobiliary Surgery, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou, China.

ABSTRACT
Dysregulation of microRNAs (miRs) is involved in carcinogenesis. Deregulation of miR-211 has recently been observed in many tumors, but its function in hepatocellular carcinoma (HCC) is still unknown. Here we found that miR-211 was decreased in HCC cancer tissues compared with adjacent normal tissues. We also found that overexpression of miR-211 repressed proliferation and invasion in HepG2 and SMMC7721 cells. Luciferase reporter assays and western blot indicated that special AT-rich sequence-binding protein-2 (SATB2), is a direct target of miR-211. The expression of SATB2 was upregulated in HCC cancer tissues and cell lines and miR-211 levels inversely correlated with SATB2 levels in HCC. Importantly, SATB2 rescued the miR-211-mediated inhibition of cell invasion and proliferation. Finally, reintroduction of miR-211 repressed tumor formation of HCC in xenograft mice. This study provides insights into molecular mechanisms that miR-211 contributed to HCC.

No MeSH data available.


Related in: MedlinePlus