Reduction of galectin-3 expression reduces pituitary tumor cell progression

Huang, Chui-Xue; Zhao, Jingyang; Zou, Wentao; Li, J.J.; Wang, P.C.; Liu, C.H.; Wang, Y.B.

doi:10.4238/2014.august.29.11

Cited by 6 publications

(3 citation statements)

References 17 publications

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“…Similar findings have been reported in other studies; Zheng et al (21) demonstrated that downregulation of galectin-3 inhibited the proliferation of hepatocellular carcinoma cells. Furthermore, Huang et al (22) found that inhibition of galectin-3 expression by siRNA suppressed cell proliferation and induced cell apoptosis of pituitary tumor cells. In addition, galectin-3 was found to be involved in the regulation of cell cycle progression; Wang et al (23) showed that galectin-3 was involved in the regulation of prostate cancer cell growth and apoptosis by modulating the expression of p21, an important regulator in cell cycle progression.…”

Section: Discussionmentioning

confidence: 99%

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Lei

et al. 2015

Molecular Medicine Reports

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Osteosarcoma (OS) is the most common malignant tumor of bone. It has recently been demonstrated that galectin-3, a multifunctional β-galactoside-binding, is significantly upregulated in OS tissues, and is correlated with its progression and metastasis. However, the detailed role of galectin‑3 in the regulation of cellular biological processes in OS cells has remained to be elucidated. The present study reported that the mRNA and protein levels of galectin‑3 were significantly increased in OS tissues compared to those in their matched normal adjacent tissues. Furthermore, galectin‑3 was upregulated in three OS cell lines, Saos‑2, MG63 and U2OS, when compared with that in the human osteoblast cell line hFOB1.19. Knockdown of galectin‑3 by galectin‑3‑specific small interfering RNA markedly inhibited OS‑cell proliferation and induced cell apoptosis. Furthermore, silencing of galectin‑3 expression significantly inhibited OS cell migration and invasion, accompanied with a marked decrease in the protein expression of matrix metalloproteinase 2 and ‑9. Mechanistic investigation suggested that the mitogen‑activated protein kinase kinase/extracellular signal‑regulated protein kinase signaling pathway may be involved in the galectin‑3‑mediated OS cell invasion. In conclusion, the present study was the first to report that silencing of galectin‑3 inhibited the malignant phenotypes of osteosarcoma in vitro. Therefore, galectin-3 may serve as a potential therapeutic target for OS.

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Section: Discussionmentioning

confidence: 99%

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Lei

et al. 2015

Molecular Medicine Reports

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“…16 Similar results were also observed in human breast cancer and human pituitary adenoma cells. 17 T cells infected with human T-cell leukemia virus type I expressed high levels of Gal-3 and displayed higher growth rates than control transfectants. 18 In our study, we used shRNA to knockdown Gal-3 expression to a level of 10% of normal group.…”

Section: Discussionmentioning

confidence: 99%

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

Sun

et al. 2016

Exp Biol Med (Maywood)

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Galectins are thought to be prognosticators for survival in renal cell cancer. However, the biological activity of galectin-3 (Gal-3) in renal carcinoma cells is still debated. In this study, immunohistochemical staining confirmed a high expression of Gal-3 in tumor tissue from renal cell carcinoma. Critically, Gal-3 expression was related to tumor cell differentiation. Consistent with Gal-3 expression in renal cell cancer, strong expression of Gal-3 was also observed in several renal tumor cell lines but not in normal renal cells. A Gal-3 high-expression cell line Caki-1 was chosen to study the biological activity of Gal-3. Using short hairpin RNA method, Gal-3 expression in Caki-1 cells was knocked down. We evidenced that Gal-3 knockdown inhibited cell proliferation and invasion, induced Caspase-3-dependent apoptosis and arrested cell cycle at G1 phase. Mechanically, Cyclin D1 expression decreased, but p27 increased after Gal-3 knockdown. Taken together, these results suggest that Gal-3 is related to the development of renal cell cancer and could serve as a target to therapy renal cell cancer.

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“…Gal-3, a β-galactoside-binding protein, is one of the most frequently investigated members of the galectin family. Gal-3 is involved in normal biological processes including cell growth, differentiation and cell adhesion, but is also involved in the progression of a number of types of cancer, including pituitary, thyroid, colon and breast cancer ( 5 – 8 ). However, the mechanisms underlying the involvement of Gal-3 in the tumorigenesis and development of pituitary adenomas remain unknown.…”

Section: Introductionmentioning

confidence: 99%

The role of galectin-3 in the tumorigenesis and progression of pituitary tumors

Diao

Liu

et al. 2018

Oncol Lett

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Galectin-3 (Gal-3), a β-galactoside-binding protein, has been implicated in cell proliferation, cell adhesion, and the progression and metastasis of various types of cancer. The present study investigated the involvement of Gal-3 in the tumorigenesis and progression of pituitary tumors using three rat pituitary tumor cell lines. Following transfection with Gal-3 expression and interference vectors, the impact of Gal-3 on proliferation, apoptosis and migration of pituitary tumor cells was been investigated. Meanwhile, BCL2 associated X, apoptosis regulator (Bax), caspase-3 and matrix metalloproteinase 7 (MMP7) protein expression levels were analyzed by western blotting. The results of the present study revealed that Gal-3 expression in GH3 and GH4C1 cells was higher than in RC-4B/C cells. Furthermore, Gal-3 was demonstrated to promote the proliferation and migration of GH3 and GH4C1 cells, and inhibit cell apoptosis. Caspase-3 and MMP7 protein expression was also increased by Gal-3, while Bax expression was decreased. These results suggested that Gal-3 serves an important function in the tumorigenesis and development of pituitary tumors, and it may be a useful target for the treatment of pituitary tumors in the future.

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Reduction of galectin-3 expression reduces pituitary tumor cell progression

Cited by 6 publications

References 17 publications

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Small interfering RNA-induced silencing of galectin-3 inhibits the malignant phenotypes of osteosarcoma in vitro

Antitumor effects of galectin-3 inhibition in human renal carcinoma cells

The role of galectin-3 in the tumorigenesis and progression of pituitary tumors

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