Abstract

Kinesin family member C1 (KIFC1) is a minus-end-directed motor protein that is critically involved in microtubule crosslinking and spindle formation. KIFC1 is essential for supernumerary centrosomes, and it is associated with the initiation and progression of cancers. In the present study, we initially reviewed the The Cancer Genome Atlas database and observed that KIFC1 is abundantly expressed in most types of tumors. We then analyzed the gene alteration profiles, protein expressions, prognoses, and immune reactivities of KIFC1 in more than 10,000 samples from several well-established databases. In addition, we conducted a gene set enrichment analysis to investigate the potential mechanisms for the roles of KIFC1 in carcinogenesis. The pan-cancer analysis of KIFC1 demonstrates significant statistical correlations of the KIFC1 expression with the clinical prognoses, the oncogenic signature gene sets, the myeloid-derived suppressor cell infiltration, the ImmunoScore, the immune checkpoints, the microsatellite instabilities, and the tumor mutational burdens across multiple tumors. These data may provide important information on the understanding of the role and mechanisms of KIFC1 in carcinogenesis and immunotherapy, as well as on the clinical progression of a variety of cancers.

Highlights

  • The kinesin family member C1 (KIFC1) gene was first identified within a segment centromeric to the class II gene region of the human major histocompatibility complex in1992 [1]

  • Recent studies have shown that KIFC1 is highly expressed in prostate cancer, hepatocellular carcinoma, serous ovarian adenocarcinomas, non-small cell lung cancer, renal cell carcinoma, triplenegative breast cancer, and that it is associated with poor prognoses [12–17]

  • (1) Theacross expression level of nificantly in study, tumor we tissues than in normal most types of KIFC1 tumorswas in significantly higher in tumor tissues than in normal tissues across most types of tumors the TCGA cohort; (2) The total KIFC1 protein expression was higher in the primary canin thethan cohort; (2)tissues

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Summary

Introduction

The kinesin family member C1 (KIFC1) gene was first identified within a segment centromeric to the class II gene region of the human major histocompatibility complex in1992 [1]. KIFC1, which is a microtubule-binding protein of the kinesin-14 family, is a minus-end-directed motor protein that is critically involved in microtubule crosslinking and spindle assembly in mammalian cells [3,4]. KIFC1 is essential for supernumerary centrosomes, which is known as “centrosome amplification”, and it promotes the multipolar spindle formation in cells. Recent studies have shown that KIFC1 is highly expressed in prostate cancer, hepatocellular carcinoma, serous ovarian adenocarcinomas, non-small cell lung cancer, renal cell carcinoma, triplenegative breast cancer, and that it is associated with poor prognoses [12–17]. KIFC1 is associated with docetaxel resistance in breast cancer and prostate cancer [18,19]. Some studies suggest that KIFC1 may be involved in tumor recurrence [13,20]. The depletion of KIFC1 leads to dramatic increases in multipolar anaphases, and to the selective cell

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