Colorectal cancer (CRC) is the second leading cause of cancer-related mortality worldwide. Kinesin Family Member C1 (KIFC1) has been proposed as a promising therapeutic target due to its pivotal role in centrosome clustering to mediate cancer cell progression. This study aimed to analyze the expression and biological function of KIFC1 in CRC. Immunohistochemically, 67 (52%) of 129 CRC cases were positive for KIFC1 and statistically associated with poorer overall survival. KIFC1 small interfering RNA (siRNA)-transfected cells demonstrated lower cell proliferation as compared to the negative control cells. A specific KIFC1 inhibitor, kolavenic acid analog (KAA) drastically inhibited CRC cell proliferation. Microarray analysis revealed that KAA-treated CRC cells presented reduced ZW10 interacting kinetochore protein (ZWINT) expression as compared to control cells. Immunohistochemical analysis demonstrated that 61 (47%) of 129 CRC cases were positive for ZWINT and ZWINT expression was significantly correlated with KIFC1 expression. ZWINT-positive cases exhibited significantly worse overall survival. KIFC1 siRNA-transfected cells showed reduced ZWINT expression while ZWINT siRNA-transfected cells decreased cell proliferation. Both KIFC1 and ZWINT knockdown cells attenuated spheroid formation ability. This study provides new insights into KIFC1 regulating ZWINT in CRC progression and its potential as a therapeutic target.
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http://dx.doi.org/10.1111/pin.13098 | DOI Listing |
Breast J
January 2025
Department of Breast and Thyroid Surgery The First Affiliated Hospital of Chongqing Medical University, No. 1 Youyi Rd, Chongqing 400016, China.
Background: The purpose of this study was to analyze SUMO activating enzyme subunit 1 (SAE1) expression in breast cancer (BC). Through bioinformatics analysis and in vitro experiments, the biological function and possibly associated signal pathways of SAE1 in BC were further analyzed.
Methods: Bioinformatics analysis was applied to analyze SAE1 expression in BC and normal breast tissues, its relationship with clinicopathologic characteristics and prognosis in BC patients, and data from the Cancer Genome Atlas database and Gene Expression Omnibus dataset.
Cancer Genomics Proteomics
December 2024
Department of Premedical Science, College of Medicine, Chosun University, Gwangju, Republic of Korea
Background/aim: Replication factor C subunit 3 (RFC3) is a critical component of the replication factor C complex, which is essential for DNA replication and repair. Recent studies have highlighted the RFC3's significance in various cancer types. Herein, we aimed to elucidate its biological role in cervical cancer.
View Article and Find Full Text PDFNeurosci Lett
January 2025
Department of Anesthesiology, The Affiliated Yixing Hospital of Jiangsu University, Yixing, Jiangsu, China. Electronic address:
Postoperative cognitive dysfunction (POCD) is a common cognitive challenge faced by older adults. One of the key contributors to the development of POCD is neuroinflammation induced by microglia. Resveratrol has emerged as a promising candidate for the prevention of cognitive decline.
View Article and Find Full Text PDFObjective: Ankylosing spondylitis (AS) patients often present with microscopic signs of gut inflammation. We used proteomic techniques to identify the differentially expressed proteins (DEPs) in the colon tissues of patients with AS and patients with gut inflammation, and then used investigated the influence of NMRAL1 protein on inflammatory cytokines to explore its potential role in the pathogenesis of AS and gut inflammation.
Methods: Colonic mucosal tissues were collected from four different groups: healthy individuals (group A), patients with gut inflammation only (group B), patients with AS only (group C), and patients with AS combined with gut inflammation (group D).
Biochem Biophys Res Commun
December 2024
Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Yamashiro-cho, Tokushima, 770-8514, Japan. Electronic address:
Chronic exposure to arsenic has been shown to induce carcinogenesis in multiple organs, but the mechanisms underlying the multi-organ carcinogenicity of arsenic remain unknown. We here examined whether arsenic affects the amount of sialic acid on the cellular surface of immortalized HaCaT cells rather than cancerous cells to clarify the process of arsenic-induced carcinogenesis, since sialic acid is known to assist cancer cells in suppressing attacks by natural killer (NK) cells. Our results indicated that exposure to arsenite (As(III)) increases the amounts of sialic acid on the cell surface of HaCaT cells.
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