Rabindranath Bera^1,#, Yotaro Ochi^2,3, Ying-Jung Huang¹, Ming-Chung Kuo^1,4, Kenichi Yoshida⁵, Seishi Ogawa², Lee-Yung Shih^1,4,*

Oncology Research, Vol.34, No.1, 2026, DOI:10.32604/or.2025.070259 - 30 December 2025

Abstract Background: Breakpoint Cluster Region-Abelson (BCR::ABL1) fusion protein is essential in the pathogenesis of chronic myeloid leukemia (CML); however, the chronic-to-blast phase transformation remains elusive. We identified novel kinesin light chain 2 (KLC2) mutations in CML-myeloid blast phase patients. We aimed to examine the functional role of KLC2 mutations in leukemogenesis. Methods: To evaluate the biological role of KLC2 mutants (MT) in CML cells, we expressed KLC2-MT in different human CML cell lines harboring BCR::ABL1 and performed immunoblot, immunofluorescence, cell proliferation, differentiation, and apoptosis; Tyrosine kinase inhibitor (TKI)-drug activities; and clonogenic assays for in vitro functional analyses. We co-expressed KLC2-MT… More >

CHUYING ZHOU¹, MINEKO KENGAKU^1,2,*

BIOCELL, Vol.46, No.11, pp. 2357-2361, 2022, DOI:10.32604/biocell.2022.021050 - 07 July 2022

Abstract Neuronal migration is a fundamental process of mammalian brain development. In migrating neurons, the nuclear membrane protein Nesprin-2 has been shown to serve as an adaptor to pull the nucleus along microtubule tracks. Current evidence has shown that Nesprin-2 binds to both the minus-end-directed motor dynein as well as the plus-end-directed motor kinesin. However, translocation of neuronal nucleus has long been thought to be primarily driven by dynein motors. Intriguing questions could be raised about the role of kinesin in nuclear transport and how the activities of opposing motors are coordinated through interactions with Nesprin. More >

Gang Li^*, Tie Chong^*, Jie Yang^†, Hongliang Li^*, Haiwen Chen^*

Oncology Research, Vol.27, No.1, pp. 125-137, 2019, DOI:10.3727/096504018X15213115046567

Abstract KIFC1 (kinesin family member C1) plays a critical role in clustering of extra centrosomes in various cancer cells and thus could be considered as a promising therapeutic target. However, whether KIFC1 is involved in the procession of renal cell carcinoma (RCC) still remains unclear. In this study, we found that KIFC1 was upregulated in RCC tissues and is responsible for RCC tumorigenesis (p<0.001). The high expression of KIFC1 correlates with aggressive clinicopathologic parameters. Kaplan–Meier analysis suggested that KIFC1 was associated with poor survival prognosis in RCC. Silencing KIFC1 dramatically resulted in inhibition of proliferation, delayed the More >