The impact of mitotic errors on cell proliferation and tumorigenesis

Abstract

Mitosis is a delicate event that must be executed with high fidelity to ensure genomic stability. Recent work has provided insight into how mitotic errors shape cancer genomes by driving both numerical and structural alterations in chromosomes that contribute to tumor initiation and progression. Here, we review the sources of mitotic errors in human tumors and their effect on cell fitness and transformation. We discuss new findings that suggest that chromosome missegregation can produce a proinflammatory environment and impact tumor responsiveness to immunotherapy. Finally, we survey the vulnerabilities exposed by cell division errors and how they can be exploited therapeutically.

Establishment of cohesion 1 homolog 2 facilitates cell aggressive behaviors and induces poor prognosis in renal cell carcinoma

“…And human express two related acetyltransferase enzymes: Esco1 and Esco2. As mentioned in the literature review, Esco1 and Esco2 are essential for chromosomal stability and many human cancers are often formed from the instability of chromosomes . Thus, increasing reports have been conducted to examine the action of ESCO1 and ESCO2 in various cancer carcinogenesis.…”

Chromosome 12p Amplification in Triple-Negative/BRCA1-Mutated Breast Cancer Associates with Emergence of Docetaxel Resistance and Carboplatin Sensitivity

“…Gene expression pathways enriched in IDB-02R model converge with those TNBCs from METABRIC featuring chr12p amplification in pathways involved in mitosis, cell cycle, and cell division. These are key biological processes in tumorigenesis and resistance acquisition (37), all of which are mediated by microtubules, kinesins, and cell division cycle-associated proteins (38,39), among others.…”

Expression of the NEK family in normal and cancer tissue: an immunohistochemical study

“…PKs regulate the cell cycle, especially at the checkpoint process, are considered interesting therapeutic targets in cancer [2]. Failures at these control points may lead to the development of tumour cells that show altered division rates and may present accumulation of DNA errors (for review [3]). In a large-scale screening of in situ hybridization on tissue microarrays, around 20% of the serine/threonine kinases analysed exhibited altered levels of transcripts in tumours [4].…”