Suppression of motor protein KIF3C expression inhibits tumor growth and metastasis in breast cancer by inhibiting TGF-β signaling. Issue 1 (1st November 2015)
- Record Type:
- Journal Article
- Title:
- Suppression of motor protein KIF3C expression inhibits tumor growth and metastasis in breast cancer by inhibiting TGF-β signaling. Issue 1 (1st November 2015)
- Main Title:
- Suppression of motor protein KIF3C expression inhibits tumor growth and metastasis in breast cancer by inhibiting TGF-β signaling
- Authors:
- Wang, Chengqin
Wang, Chenggang
Wei, Zhimin
Li, Yujun
Wang, Wenhong
Li, Xia
Zhao, Jing
Zhou, Xuan
Qu, Xun
Xiang, Fenggang - Abstract:
- Highlights: KIF3C over-expressed in breast cancer. High expression of KIF3C was associated with tumor metastasis and recurrence. Silencing of KIF3C suppressed breast cancer cell proliferation and invasion through TGF-β signaling. Abstract: Breast cancer is the most common cause of death among women. KIF3C, a member of kinesin superfamily, functions as a motor protein involved in axonal transport in neuronal cells. To explore the expression, regulation and mechanism of KIF3C in breast cancer, 4 breast cancer cell lines and 93 cases of primary breast cancer and paired adjacent tissues were examined. Immunohistochemistry, Real Time Polymerase Chain Reaction (RT-PCR), Western blot, flow cytometry, short hairpin RNA (shRNA) interference, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), colony formation techniques and xenograft mice model were used. We found that KIF3C was over-expressed in breast cancer tissues and such high KIF3C expression was also associated with tumor recurrence and lymph node metastasis. Silencing of KIF3C by shRNA inhibited epithelial-mesenchymal transition and metastasis by inhibiting TGF-β signaling and suppressed breast cancer cell proliferation through inducing G2 /M phase arrest. The tumor size was smaller and the number of lung metastatic nodules was less in KIF3C depletion MDA-MB-231 cell xenograft mice than in negative control group. These results suggested that high expression of KIF3C in breast cancer may be associated withHighlights: KIF3C over-expressed in breast cancer. High expression of KIF3C was associated with tumor metastasis and recurrence. Silencing of KIF3C suppressed breast cancer cell proliferation and invasion through TGF-β signaling. Abstract: Breast cancer is the most common cause of death among women. KIF3C, a member of kinesin superfamily, functions as a motor protein involved in axonal transport in neuronal cells. To explore the expression, regulation and mechanism of KIF3C in breast cancer, 4 breast cancer cell lines and 93 cases of primary breast cancer and paired adjacent tissues were examined. Immunohistochemistry, Real Time Polymerase Chain Reaction (RT-PCR), Western blot, flow cytometry, short hairpin RNA (shRNA) interference, 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), colony formation techniques and xenograft mice model were used. We found that KIF3C was over-expressed in breast cancer tissues and such high KIF3C expression was also associated with tumor recurrence and lymph node metastasis. Silencing of KIF3C by shRNA inhibited epithelial-mesenchymal transition and metastasis by inhibiting TGF-β signaling and suppressed breast cancer cell proliferation through inducing G2 /M phase arrest. The tumor size was smaller and the number of lung metastatic nodules was less in KIF3C depletion MDA-MB-231 cell xenograft mice than in negative control group. These results suggested that high expression of KIF3C in breast cancer may be associated with the tumor progression and metastasis. … (more)
- Is Part Of:
- Cancer letters. Volume 368:Issue 1(2016)
- Journal:
- Cancer letters
- Issue:
- Volume 368:Issue 1(2016)
- Issue Display:
- Volume 368, Issue 1 (2016)
- Year:
- 2016
- Volume:
- 368
- Issue:
- 1
- Issue Sort Value:
- 2016-0368-0001-0000
- Page Start:
- 105
- Page End:
- 114
- Publication Date:
- 2015-11-01
- Subjects:
- KIF3C -- Breast cancer -- shRNA -- Metastasis -- TGF-β signaling
Cancer -- Periodicals
Neoplasms -- Periodicals
Cancer -- Périodiques
Electronic journals
616.994 - Journal URLs:
- http://www.sciencedirect.com/science/journal/03043835/ ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.canlet.2015.07.037 ↗
- Languages:
- English
- ISSNs:
- 0304-3835
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3046.485000
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- 10975.xml