MicroRNA-2053 involves in the progression of esophageal cancer by targeting KIF3C

Yao, Wenjian; Jing, Xue; Liu, Xu; Li, Saisai; Li, Wei

doi:10.1080/15384101.2021.1929675

Cited by 12 publications

(6 citation statements)

References 47 publications

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“… 31 , 32 It is even considered as a potential therapeutic target for solid tumors; for example, reducing the expression of KIF3C inhibits the proliferation and metastasis of breast cancer. 31 , 33 The above studies suggest that high expression of KIF3C may cause a disruption of cell division leading to tumorigenesis. The KIF3C c.G1229A mutation led to a significant increase in KIF3C expression at the mRNA and protein levels, and also significantly increased cell proliferation and migration, showing the efficacy of gain of function.…”

Section: Discussionmentioning

confidence: 99%

Double heterozygous pathogenic mutations in KIF3C and ZNF513 cause hereditary gingival fibromatosis

Chen,

Xu,

Chen

et al. 2023

Int J Oral Sci

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Hereditary gingival fibromatosis (HGF) is a rare inherited condition with fibromatoid hyperplasia of the gingival tissue that exhibits great genetic heterogeneity. Five distinct loci related to non-syndromic HGF have been identified; however, only two disease-causing genes, SOS1 and REST, inducing HGF have been identified at two loci, GINGF1 and GINGF5, respectively. Here, based on a family pedigree with 26 members, including nine patients with HGF, we identified double heterozygous pathogenic mutations in the ZNF513 (c.C748T, p.R250W) and KIF3C (c.G1229A, p.R410H) genes within the GINGF3 locus related to HGF. Functional studies demonstrated that the ZNF513 p.R250W and KIF3C p.R410H variants significantly increased the expression of ZNF513 and KIF3C in vitro and in vivo. ZNF513, a transcription factor, binds to KIF3C exon 1 and participates in the positive regulation of KIF3C expression in gingival fibroblasts. Furthermore, a knock-in mouse model confirmed that heterozygous or homozygous mutations within Zfp513 (p.R250W) or Kif3c (p.R412H) alone do not led to clear phenotypes with gingival fibromatosis, whereas the double mutations led to gingival hyperplasia phenotypes. In addition, we found that ZNF513 binds to the SOS1 promoter and plays an important positive role in regulating the expression of SOS1. Moreover, the KIF3C p.R410H mutation could activate the PI3K and KCNQ1 potassium channels. ZNF513 combined with KIF3C regulates gingival fibroblast proliferation, migration, and fibrosis response via the PI3K/AKT/mTOR and Ras/Raf/MEK/ERK pathways. In summary, these results demonstrate ZNF513 + KIF3C as an important genetic combination in HGF manifestation and suggest that ZNF513 mutation may be a major risk factor for HGF.

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Section: Discussionmentioning

confidence: 99%

Double heterozygous pathogenic mutations in KIF3C and ZNF513 cause hereditary gingival fibromatosis

Chen,

Xu,

Chen

et al. 2023

Int J Oral Sci

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“…The downregulated hsa-miR-2053 increases KIF3C expression and activates the PI3K/AKT signaling pathway, causing esophageal cancer cells to proliferate, undergo apoptosis, migrate, and invade. 71 A previous study revealed that hsa-miR-2053 expression is upregulated in patients with malignant pleural mesothelium (MPM). Further, they concluded that hsa-miR-2053 is an independent prognostic factor of MPM.…”

Section: Discussionmentioning

confidence: 99%

Deciphering the miRNA–mRNA Interaction Landscape between Breast Cancer and Triple-Negative Breast Cancer: An Integrated Bioinformatics Approach

Balasundaram,

Mitra,

Tayubi

et al. 2024

ACS Omega

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Breast cancer (BC) is globally recognized as the second most prevalent form of cancer. It predominantly affects women and can be categorized into distinct types based on the overexpression of specific cancer receptors.The key receptors implicated in this context are the human epidermal growth factor receptor-2 (HER2), estrogen receptor (ER), and progesterone receptor (PR), alongside a particularly intricate subclass known as triple-negative breast cancer (TNBC). This subclassification is critical for the stratification of breast cancer and informs therapeutic decision-making processes. Due to a lack of therapeutic targets, such as growth factor receptors, TNBC is the most aggressive type. Hence, identifying targetable regulators such as miRNAs could pave the way for potential therapeutic interventions. To identify common differentially expressed mRNAs (DE-mRNAs) in BC, including TNBC, we leveraged two data sets from the GEO collection and The Cancer Genome Atlas (TCGA). Significant DE-mRNAs were identified through PPI, MCODE, CytoNCA, and CytoHubba analyses. Following this, miRNAs were predicted using mirDIP. We utilized GSE42568, GSE185645, and TCGA and identified 159 common DE-mRNAs. Using Cytoscape plug-ins, we identified the 10 most significant DE-mRNAs in BC. Using mirDIP, target miRNAs for 10 DE-mRNAs were identified. We conducted an advanced analysis on the TNBC GEO data set (GSE45498) to corroborate the significance of shared DE-mRNAs and DE-miRNAs in TNBC. We identified four downregulated DE-miRNAs, including hsa-miR-802, hsa-miR-1258, hsa-miR-548a-3p, and hsa-miR-2053, significantly associated with TNBC. Our study revealed significant miRNA−mRNA interactions, specifically hsa-miR-802/ MELK, hsa-miR-1258/NCAPG, miR-548a-3p/CCNA2, and hsa-miR-2053/NUSAP1, in both BC and TNBC. The observed downregulation of hsa-miR-548a-3p is associated with diminished survival rates in BC patients, emphasizing their potential utility as prognostic indicators. Furthermore, the differential expression of mRNAs, including CCNB2, UBE2C, MELK, and KIF2C, correlates with reduced survival outcomes, signifying their critical role as potential targets for therapeutic intervention in both BC and TNBC. These findings highlight specific regulatory mechanisms that are potentially crucial for understanding and treating these cancer types.

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“…MicroRNAs (miRNAs) are small non-coding RNA with 18-22 nucleotides in length, and their expression can be inhibited by targeting the genes. Studies have demonstrated that micorRNA-2053 negatively regulates tumor proliferation, invasion, and migration by targeting KIF3C in esophageal cancer [18] . Previously, we found that KIF3C mRNA levels were significantly upregulated in non-small cell lung cancer tissues through tumor database integration analysis, and correlated with poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Knockdown of KIF3C Inhibits Epithelial-Mesenchymal Transition in Lung Cancer Cells A549

Liu

Hao

et al. 2022

JCNR

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The objective of this study is to reveal the role of KIF3C gene in the proliferation of lung cancer cells, and the regulation of epithelial mesenchymal transition (EMT) of tumor cells. The plate clone formation assay and cell scratch assay were used in this study to detect the changes of cell proliferation and migration ability after siKIF3C interference, while EMT-related protein expression after KIF3C downregulation was detected by Western blot. The cell clone formation assay showed that the number of clones of lung cancer cells A549 was significantly reduced after transfected with siKIF3C (P<0.05); The scratch assay showed that the healing ability of cells was significantly reduced after transfected with siKIF3C (P<0.05); Western blot protein analysis revealed that the levels of EMT-related proteins, N-cadherin, Vimentin, Snail, and Slug were significantly down-regulated (P<0.05), however, E-cadherin protein levels were up-regulated after siKIF3C interference. In conclusion, KIF3C may promote the proliferation and invasive ability of lung cancer cells A549 through EMT.

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MicroRNA-2053 involves in the progression of esophageal cancer by targeting KIF3C

Cited by 12 publications

References 47 publications

Double heterozygous pathogenic mutations in KIF3C and ZNF513 cause hereditary gingival fibromatosis

Double heterozygous pathogenic mutations in KIF3C and ZNF513 cause hereditary gingival fibromatosis

Deciphering the miRNA–mRNA Interaction Landscape between Breast Cancer and Triple-Negative Breast Cancer: An Integrated Bioinformatics Approach

Knockdown of KIF3C Inhibits Epithelial-Mesenchymal Transition in Lung Cancer Cells A549

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