RETRACTED ARTICLE: Kinesin family member 15 can promote the proliferation of glioblastoma

Leibo Wang; Xuebin Zhang; Jun Liu; Qingjun Liu; Leibo Wang; Xuebin Zhang; Jun Liu; Qingjun Liu

doi:10.3934/mbe.2022384

Mathematical Biosciences and Engineering

2022, Volume 19, Issue 8: 8259-8272. doi: 10.3934/mbe.2022384

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Research article

RETRACTED ARTICLE: Kinesin family member 15 can promote the proliferation of glioblastoma

1.
Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, China
2.
Department of Pathology, Tianjin Huanhu Hospital, Tianjin 300350, China

Retraction published on 22 April 2024, see MBE 2024, 21(4), 5686.

Academic Editor: Leyi Wei

Received: 25 March 2022 Revised: 18 April 2022 Accepted: 08 May 2022 Published: 06 June 2022

Glioblastoma is one of the most dangerous tumors for patients in clinical practice at present, and since glioblastoma originates from the brain, it will have a serious impact on patients. Therefore, more effective clinical therapeutic targets are still needed at this stage. Kinesin family member 15 (KIF15) promotes proliferation in several cancers, but its effect on glioblastoma is unclear. In this study, differentially expressed gene analysis and network analysis were performed to identify critical genes affecting glioma progression. The samples were divided into a KIF15 high-expression group and KIF15 low-expression group, and the association between FIK15 expression level and clinical characteristics was summarized and analyzed by performing medical data analysis; the effect of KIF15 on glioblastoma cell proliferation was detected by employing colony formation and MTT assays. The effect of KIF15 on tumor growth in mice was determined. It was found that KIF15 was a potential gene affecting the progression of glioblastoma. In addition, KIF15 was highly expressed in glioblastoma tumor tissues, and KIF15 was correlated with tumor size, clinical stage and other clinical characteristics. After the KIF15 gene was knocked out, the proliferation ability of glioblastoma was significantly inhibited. KIF15 also contributed to the growth of glioblastoma tumors in mice. Therefore, we found KIF15 to be a promising clinical therapeutic target.
- glioblastoma,
- kinesin family member 15 (KIF15),
- proliferation,
- clinical characteristics,
- therapeutic target
Citation: Leibo Wang, Xuebin Zhang, Jun Liu, Qingjun Liu. RETRACTED ARTICLE: Kinesin family member 15 can promote the proliferation of glioblastoma[J]. Mathematical Biosciences and Engineering, 2022, 19(8): 8259-8272. doi: 10.3934/mbe.2022384

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Abstract

Glioblastoma is one of the most dangerous tumors for patients in clinical practice at present, and since glioblastoma originates from the brain, it will have a serious impact on patients. Therefore, more effective clinical therapeutic targets are still needed at this stage. Kinesin family member 15 (KIF15) promotes proliferation in several cancers, but its effect on glioblastoma is unclear. In this study, differentially expressed gene analysis and network analysis were performed to identify critical genes affecting glioma progression. The samples were divided into a KIF15 high-expression group and KIF15 low-expression group, and the association between FIK15 expression level and clinical characteristics was summarized and analyzed by performing medical data analysis; the effect of KIF15 on glioblastoma cell proliferation was detected by employing colony formation and MTT assays. The effect of KIF15 on tumor growth in mice was determined. It was found that KIF15 was a potential gene affecting the progression of glioblastoma. In addition, KIF15 was highly expressed in glioblastoma tumor tissues, and KIF15 was correlated with tumor size, clinical stage and other clinical characteristics. After the KIF15 gene was knocked out, the proliferation ability of glioblastoma was significantly inhibited. KIF15 also contributed to the growth of glioblastoma tumors in mice. Therefore, we found KIF15 to be a promising clinical therapeutic target.

References

[1]	X. X. Ke, Y. Pang, K. Chen, D. Zhang, F. Wang, S. Zhu, et al., Knockdown of arsenic resistance protein 2 inhibits human glioblastoma cell proliferation through the MAPK/ERK pathway, Oncol. Rep., 40 (2018), 3313-3322. https://doi.org/10.3892/or.2018.6777 doi: 10.3892/or.2018.6777
[2]	H. Y. Li, B. B. Lv, Y. H. Bi, FABP4 accelerates glioblastoma cell growth and metastasis through Wnt10b signalling, Eur. Rev. Med. Pharmacol. Sci., 22 (2018), 7807-7818. https://doi.org/10.26355/eurrev_201811_16405 doi: 10.26355/eurrev_201811_16405
[3]	T. Mashimo, K. Pichumani, V. Vemireddy, K. J. Hatanpaa, D. K. Singh, S. Sirasanagandla, et al., Acetate is a bioenergetic substrate for human glioblastoma and brain metastases, Cell, 159 (2014), 1603-1614. https://doi.org/10.1016/j.cell.2014.11.025 doi: 10.1016/j.cell.2014.11.025
[4]	A. Vartanian, S. Agnihotri, M. R. Wilson, K. E. Burrell, P. D. Tonge, A. Alamsahebpour, et al., Targeting hexokinase 2 enhances response to radio-chemotherapy in glioblastoma, Oncotarget, 7 (2016), 69518-69535. https://doi.org/10.18632/oncotarget.11680 doi: 10.18632/oncotarget.11680
[5]	B. Huang, T. A. Dolecek, Q. Chen, C. R. Garcia, T. Pittman, J. L. Villano, Characteristics and survival outcomes associated with the lack of radiation in the treatment of glioblastoma, Med. Oncol., 35 (2018), 74. https://doi.org/10.1007/s12032-018-1134-3 doi: 10.1007/s12032-018-1134-3
[6]	Z. Shboul, L. Vidyaratne, M. Alam, S. M. S. Reza, K. M. Iftekharuddin, Glioblastoma and survival prediction, Lect. Notes Comput. Sci., 10670 (2018), 358-368. https://doi.org/10.1007/978-3-319-75238-9_31 doi: 10.1007/978-3-319-75238-9_31
[7]	J. K. Sa, S. H. Kim, J. K. Lee, H. J. Cho, Y. J. Shin, H. Shin, et al., Identification of genomic and molecular traits that present therapeutic vulnerability to HGF-targeted therapy in glioblastoma, Neuro-oncology, 21 (2019), 222-233. https://doi.org/10.1093/neuonc/noy105 doi: 10.1093/neuonc/noy105
[8]	Z. C. Zhu, J. W. Liu, K. Li, J. Zheng, Z. Q. Xiong, KPNB1 inhibition disrupts proteostasis and triggers unfolded protein response-mediated apoptosis in glioblastoma cells, Oncogene, 37 (2018), 2936-2952. https://doi.org/10.1038/s41388-018-0180-9 doi: 10.1038/s41388-018-0180-9
[9]	M. Westphal, C. L. Maire, K. Lamszus, EGFR as a target for glioblastoma treatment: An unfulfilled promise, CNS Drugs, 31 (2017), 723-735. https://doi.org/10.1007/s40263-017-0456-6 doi: 10.1007/s40263-017-0456-6
[10]	N. Hirokawa, Y, Tanaka, Kinesin superfamily proteins (KIFs): Various functions and their relevance for important phenomena in life and diseases, Exp. Cell Res., 334 (2015), 16-25. https://doi.org/10.1016/j.yexcr.2015.02.016 doi: 10.1016/j.yexcr.2015.02.016
[11]	N. Hirokawa, From electron microscopy to molecular cell biology, molecular genetics and structural biology: Intracellular transport and kinesin superfamily proteins, KIFs: Genes, structure, dynamics and functions, J. Electron Microsc., 60 (2011), 63-92. https://doi.org/10.1093/jmicro/dfr051
[12]	S. S. Siddiqui, Metazoan motor models: Kinesin superfamily in C. elegans, Traffic, 3 (2002), 20-28. https://doi.org/10.1034/j.1600-0854.2002.30104.x doi: 10.1034/j.1600-0854.2002.30104.x
[13]	H. Miki, M. Setou, K. Kaneshiro, N. Hirokawa, All kinesin superfamily protein, KIF, genes in mouse and human, Proc. Natl. Acad. Sci. U.S.A., 98 (2001), 7004-7011. https://doi.org/10.1073/pnas.111145398 doi: 10.1073/pnas.111145398
[14]	Y. M. Lee, W. Kim, Kinesin superfamily protein member 4 (KIF4) is localized to midzone and midbody in dividing cells, Exp. Mol. Med., 36 (2004), 93-97. https://doi.org/10.1038/emm.2004.13 doi: 10.1038/emm.2004.13
[15]	Z. Shen, A. R. Collatos, J. P. Bibeau, F. Furt, L. Vidali, Phylogenetic analysis of the Kinesin superfamily from physcomitrella, Front. Plant Sci., 3 (2012), 230. https://doi.org/10.3389/fpls.2012.00230 doi: 10.3389/fpls.2012.00230
[16]	K. Tang, N. H. Toda, A microtubule polymerase cooperates with the kinesin-6 motor and a microtubule cross-linker to promote bipolar spindle assembly in the absence of kinesin-5 and kinesin-14 in fission yeast, Mol. Biol. Cell, 28 (2017), 3647-3659. https://doi.org/10.1091/mbc.e17-08-0497 doi: 10.1091/mbc.e17-08-0497
[17]	T. McHugh, H. Drechsler, A. D. McAinsh, N. J. Carter, R. A. Cross, Kif15 functions as an active mechanical ratchet, Mol. Biol. Cell, 29 (2018), 1743-1752. https://doi.org/10.1091/mbc.E18-03-0151 doi: 10.1091/mbc.E18-03-0151
[18]	M. Xu, D. Liu, Z. Dong, X. Wang, X. Wang, Y. Liu, et al., Kinesin-12 influences axonal growth during zebrafish neural development, Cytoskeleton, 71 (2014), 555-563. https://doi.org/10.1002/cm.21193 doi: 10.1002/cm.21193
[19]	J. Feng, Z. Hu, H. Chen, J. Hua, R. Wu, Z. Dong, et al., Depletion of kinesin-12, a myosin-ⅡB-interacting protein, promotes migration of cortical astrocytes, J. Cell. Sci., 129 (2016), 2438-2447. https://doi.org/10.1242/jcs.181867 doi: 10.1242/jcs.181867
[20]	H. Miki, M. Setou, K. Kaneshiro, N. Hirokawa, All kinesin superfamily protein, KIF, genes in mouse and human, Proc. Natl. Acad. Sci. U.S.A., 98 (2001), 7004-7011. https://doi.org/10.1073/pnas.111145398 doi: 10.1073/pnas.111145398
[21]	J. Wang, X. Guo, C. Xie, J. Jiang, KIF15 promotes pancreatic cancer proliferation via the MEK-ERK signalling pathway, Br. J. Cancer, 117 (2017), 245-255. https://doi.org/10.1038/bjc.2017.165 doi: 10.1038/bjc.2017.165
[22]	Y. Qiao, J. Chen, C. Ma, Y. Liu, P. Li, Y. Wang, et al., Increased KIF15 expression predicts a poor prognosis in patients with lung adenocarcinoma, Cell Physiol. Biochem., 51 (2018), 1-10. https://doi.org/10.1159/000495155 doi: 10.1159/000495155
[23]	G. Harris, D. Jayamanne, H. Wheeler, C. Gzell, M. Kastelan, G. Schembri, et al., Survival Outcomes of Elderly Patients With glioblastoma multiforme in their 75th year or older treated with adjuvant therapy, Int. J. Radiat. Oncol. Biol. Phys., 98 (2017), 802-810. https://doi.org/10.1016/j.ijrobp.2017.02.028 doi: 10.1016/j.ijrobp.2017.02.028
[24]	K. K. Jain, A critical overview of targeted therapies for glioblastoma, Front. Oncol., 8 (2018), 419. https://doi.org/10.3389/fonc.2018.00419 doi: 10.3389/fonc.2018.00419
[25]	Y. Zheng, N. Gao, Y. L. Fu, B. Y. Zhang, X. L. Li, P. Gupta, et al., Generation of regulable EGFRvⅢ targeted chimeric antigen receptor T cells for adoptive cell therapy of glioblastoma, Biochem. Biophys. Res. Commun., 507 (2018), 59-66. https://doi.org/10.1016/j.bbrc.2018.10.151 doi: 10.1016/j.bbrc.2018.10.151
[26]	M. Momeny, F. Moghaddaskho, N. K. Gortany, H. Yousefi, Z. Sabourinejad, G. Zarrinrad, et al., Blockade of vascular endothelial growth factor receptors by tivozanib has potential anti-tumour effects on human glioblastoma cells, Sci. Rep., 7 (2017), 44075. https://doi.org/10.1038/srep44075 doi: 10.1038/srep44075
[27]	E. G. Sturgill, S. R. Norris, Y. Guo, R. Ohi, Kinesin-5 inhibitor resistance is driven by kinesin-12, J. Cell. Biol., 213 (2016), 213-227. https://doi.org/10.1083/jcb.201507036 doi: 10.1083/jcb.201507036
[28]	C. Müller, D. Gross, V. Sarli, M. Gartner, A. Giannis, G. Bernhardt, et al., Inhibitors of kinesin Eg5: Antiproliferative activity of monastrol analogues against human glioblastoma cells, Cancer Chemother. Pharmacol., 59 (2007), 157-164. https://doi.org/10.1007/s00280-006-0254-1 doi: 10.1007/s00280-006-0254-1
[29]	A. I. Marcus, U. Peters, S. L. Thomas, S. Garrett, A. Zelnak, T. M. Kapoor, et al., Mitotic kinesin inhibitors induce mitotic arrest and cell death in Taxol-resistant and sensitive cancer cells, J. Biol. Chem., 280 (2005), 11569-11577. https://doi.org/10.1074/jbc.M413471200 doi: 10.1074/jbc.M413471200
[30]	D. W. Buster, D. H. Baird, W. Yu, J. M. Solowska, M. Chauviere, A. Mazurek, Expression of the mitotic kinesin Kif15 in postmitotic neurons: Implications for neuronal migration and development, J. Neurocytol., 32 (2003), 79-96. https://doi.org/10.1023/A:1027332432740 doi: 10.1023/A:1027332432740
[31]	B. Stangeland, A. A. Mughal, Z. Grieg, C. J. Sandberg, M. Joel, S. Nygard, et al., Combined expressional analysis, bioinformatics and targeted proteomics identify new potential therapeutic targets in glioblastoma stem cells, Oncotarget, 6 (2015), 26192-26215. https://doi.org/10.18632/oncotarget.4613 doi: 10.18632/oncotarget.4613
[32]	O. Rath, F. Kozielski, Kinesins and cancer, Nat. Rev. Cancer, 12 (2012), 527-539. https://doi.org/10.1038/nrc3310 doi: 10.1038/nrc3310
[33]	G. Bergnes, K. Brejc, L. Belmont, Mitotic kinesins: Prospects for antimitotic drug discovery, Curr. Top. Med. Chem., 5 (2005), 127-145. https://doi.org/10.2174/1568026053507697 doi: 10.2174/1568026053507697
[34]	Z. Z. Wang, J. Yang, B. H. Jiang, J. B. Di, P. Gao, L. Peng, et al., KIF14 promotes cell proliferation via activation of Akt and is directly targeted by miR-200c in colorectal cancer, Int. J. Oncol., 53 (2018), 1939-1952. https://doi.org/10.3892/ijo.2018.4546 doi: 10.3892/ijo.2018.4546
[35]	X. Zhao, L. L. Zhou, X. Li, J. Ni, P. Chen, R. Ma, Overexpression of KIF20A confers malignant phenotype of lung adenocarcinoma by promoting cell proliferation and inhibiting apoptosis, Cancer Med., 7 (2018), 4678-4689. https://doi.org/10.1002/cam4.1710 doi: 10.1002/cam4.1710
[36]	Y. Teng, B. Guo, X. Mu, S. Liu, KIF26B promotes cell proliferation and migration through the FGF2/ERK signaling pathway in breast cancer, Biomed. Pharmacother., 108 (2018), 766-773. https://doi.org/10.1016/j.biopha.2018.09.036 doi: 10.1016/j.biopha.2018.09.036
[37]	Q. Y. Wang, B. Han, W. Huang, C. J. Qi, F. Liu, Identification of KIF15 as a potential therapeutic target and prognostic factor for glioma, Oncol. Rep., 43 (2020), 1035-1044. https://doi.org/10.3892/or.2020.7510 doi: 10.3892/or.2020.7510

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