Stable gene-silence of Kif2a synergistic with 5-fluorouracil suppresses oral tongue squamous cell carcinoma growth in vitro and in vivo

Wang, Cheng-Qin; Li, Yujun; Wei, Zhimin; Zhu, Changjun; Qu, Xun; Fang, Wei; Xing, Xiaoming; Yu, Wei

doi:10.1016/j.oooo.2013.01.028

Cited by 9 publications

(8 citation statements)

References 18 publications

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“…A previous study demonstrated that the silencing of KIF2A significantly inhibits the growth and invasion of oral tongue squamous cell carcinoma, which suggested that KIF2A may regulate the viability and invasion of cancer cells (29). In the present study, 5-8F cell proliferation decreased and apoptosis increased in the KIF2A siRNA group compared with the control groups.…”

Section: Discussionsupporting

confidence: 57%

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

Zhang

Liu

et al. 2019

Oncol Lett

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Nasopharyngeal carcinoma (NPC) is a common tumor in south China. Kinesin family member 2A (KIF2A) belongs to the kinesin-13 family and is associated with the growth and invasion of a number of different types of human cancer, including ovarian, breast and prostate cancer. The aim of the present study was to evaluate the expression of KIF2A in NPC and explore the relationship between KIF2A and the basic characteristics of 5-8F cells. Immunohistochemistry was performed on tissues from 97 patients with NPC to assess KIF2A protein expression. KIF2A was knocked down by a specific short interfering (si)RNA in 5-8F cell lines. Cell proliferation, apoptosis and cycle were analyzed by MTT assay and flow cytometry. The invasive ability and angiogenesis were evaluated by Matrigel assay and reverse transcription-quantitative PCR. The level of KIF2A was associated with the growth and migration of primary tumor, nodal status and tumor stage. The viability of KIF2A-knockdown cells was decreased compared with that of the control cells. The number of apoptotic cells, as well as the percentage of cells in the G0/G1 phase, was higher in the KIF2A siRNA group compared with the control group. The invasive and angiogenetic ability of 5-8F cells in the KIF2A siRNA group was decreased compared with the control group. In conclusion, the expression of KIF2A correlated with the poor clinicopathological features in NPC. Therefore, KIF2A may serve an important role in the progression of NPC and proliferation of 5-8F cells, which might present a potential therapeutic target for patients with NPC.

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Section: Discussionsupporting

confidence: 57%

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

Zhang

Liu

et al. 2019

Oncol Lett

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“…The prevalence of elevated KIF2A expression was increased in lymphoma tissues compared with reactive hyperplasia, indicating that KIF2A may contribute to the malignant transformation of DLBCL. These observations are consistent with those from other tumors [ 11 , 20 , 21 ]. Additionally, the overexpression of KIF2A was related to Ann Arbor stage and high-risk IPI stratification in patients with DLBCL.…”

Section: Discussionsupporting

confidence: 93%

“…Another study showed that overexpression of KIF2A promoted metastasis and invasion of SCCOT, indicating that KIF2A overexpression is unfavorable for predicting the prognosis of SCCOT [ 20 ]. Notably, both in vivo and in vitro, treatment with KIF2A RNAi remarkably enhanced the sensitivity of SCCOT cells to 5-FU [ 21 ], suggesting that targeting KIF2A can overcome drug resistance and improve the treatment of tumors. In human epithelial ovarian cancer, overexpression of KIF2A was found in tumor tissues, and KIF2A conferred increased invasive and metastatic potential to tumor cells [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

High KIF2A expression predicts unfavorable prognosis in diffuse large B cell lymphoma

et al. 2017

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Kinesin family member 2A (KIF2A), a conserved motor protein, plays a critical role in the pathogenesis and prognosis of several malignant tumors. The aim of the present study was to investigate KIF2A expression in diffuse large B cell lymphoma (DLBCL), evaluate the association between KIF2A expression and the clinical parameters of the disease, and determine its prognostic value. KIF2A expression was evaluated in 134 DLBCL and 57 reactive hyperplasia samples using immunohistochemistry on a tissue microarray. The correlations between KIF2A expression with clinical parameters and prognosis were estimated using univariate and multivariate analyses. The expression of KIF2A was significantly higher in DLBCL tissue samples compared with those from subjects with reactive hyperplasia (P=0.002). Furthermore, increased expression of KIF2A protein in DLBCL was related to Ann Arbor stage (P=0.027) and international prognostic index (IPI) score (P=0.01). The survival analysis showed that KIF2A expression (P=0.016), serum LDH level (P=0.049), and IPI score (P<0.001) were independent prognostic markers for DLBCL. Our findings also confirmed that downregulating KIF2A expression decreased tumor cell viability, accompanied by downregulation of pAKT levels. Taken together, these data provide the first evidence that increased KIF2A expression predicts poor prognosis in patients with DLBCL, and a rationale for treatment of DLBCL by targeting KIF2A.

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“…KIF2A is a member of the kinesin families involved in cell mitosis and spindle assembly that is commonly recognized as being associated with human neuronal diseases . In recent years accumulated evidence has defined the oncogenic role of KIF2A in multiple human cancers, such as breast cancer, glioma and squamous cell carcinoma . In our study the oncogenic role of KIF2A in human gastric cancer was newly discovered.…”

Section: Discussionmentioning

confidence: 65%

Down‐regulation of KIF2A inhibits gastric cancer cell invasion via suppressing MT1‐MMP

Zhao

Lan

Zhang³

et al. 2018

Clin Exp Pharma Physio

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Gastric cancer accounts for a sizeable proportion of global cancer mortality with high morbidity and poor prognosis. Kinesin superfamily proteins (KIFs) are microtubule-dependent motor proteins that function as oncogenes in cancer cells, it has been discovered in recent years. Kinesin family member 2a (KIF2A), a member of the KIFs, has received attention for its role in carcinogenesis and its prognostic value in several human cancers such as breast cancer, colorectal cancer, and squamous cell carcinoma. However, the role of KIF2A in human gastric cancer remains unknown. In this study we aimed to explore the expression and biological functions of KIF2A in human gastric cancer cells, as well as to reveal its potential action mechanism. First, we found that KIF2A was markedly increased in gastric cancer cells (MKN-28, MKN-45, NCI-N87 and SGC-7901) compared to normal gastric mucosa epithelial cells (GES-1). Then KIF2A was successfully silenced in MKN-45 and SGC-7901 cells to facilitate further research into its function. We discovered that KIF2A silencing can significantly inhibit the growth and invasion of MKN-45 and SGC-7901 cells in a time-independent manner, accompanying a decreased expression of Membrane type 1-matrix metalloproteinase (MT1-MMP). When MT1-MMP was reintroduced into MKN-45 and SGC-7901 cells in the KIF2A-siRNA group, only invasion inhibition effects on MKN-45 and SGC-7901 cells induced by KIF2A silencing can be reversed. In conclusion, our study reveals that down-regulation of KIF2A can inhibit gastric cancer cell invasion by suppressing MT1-MMP.

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Stable gene-silence of Kif2a synergistic with 5-fluorouracil suppresses oral tongue squamous cell carcinoma growth in vitro and in vivo

Abstract: Our data support that Kif2a is a potential molecular target for the therapeutics of recurrent and metastatic SCCOT.

Cited by 9 publications

References 18 publications

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

Effects of KIF2A on the prognosis of nasopharyngeal carcinoma and nasopharyngeal carcinoma cells

High KIF2A expression predicts unfavorable prognosis in diffuse large B cell lymphoma

Down‐regulation of KIF2A inhibits gastric cancer cell invasion via suppressing MT1‐MMP

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