Relationships of kin17 protein expression with clinical features and prognosis of colorectal cancer

Ruan, Liqin; Jiang, Qunguang; Zhang, Haitao

doi:10.21037/tcr.2018.08.16

Cited by 4 publications

(5 citation statements)

References 14 publications

(15 reference statements)

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“…Therefore, our work demonstrates that Kin17 functions as a splicing factor in neuroblasts to regulate splicing of specific transcripts and proper localization of cell fate determinants. These findings could be potentially very helpful for further investigating underlying mechanisms of pathogenesis of various cancers, including breast, liver, colorectal, cervical, and non-small cell lung cancers that have increased levels of Kin17 expression (Zeng et al, 2011;Zhang et al, 2017aZhang et al, , 2017bKou et al, 2014;Ruan et al, 2018).…”

Section: Discussionmentioning

confidence: 95%

Kin17 drives dissociation of Mira from the centrosome in neuroblasts by regulating splicing of Flfl

Connell

Xie

Chen

et al. 2021

Preprint

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During asymmetric division of Drosophila neuroblasts, the fate determinant Prospero and its adaptor Miranda are segregated to the basal cortex through aPKC phosphorylation of Miranda and displacement from the apical cortex. Here we identify Kin17 as a novel regulator of Miranda localization during asymmetric cell division and loss of Kin17 or Protein Phosphatase 4 leads to aberrant localization of Miranda to the centrosome and cytoplasm and Prospero to the centrosome and nucleus. We report that dephosphorylation of Mira by Protein Phosphatase 4 at Serine-96 at the centrosome is required for the proper basal localization of Mira after being phosphorylated at the apical cortex. We further demonstrate that Kin17 regulates Miranda localization by promoting splicing of the transcript of a PP4 component Falafel. Taken together, our work reveals a novel mechanism that ensures proper basal localization of Miranda by preventing its aberrant localization to the centrosome during the asymmetric division.SummaryConnell et al. show that proper segregation of cell fate determinant Miranda requires PP4-mediated dissociation of Miranda from the centrosome/spindle in Drosophila neuroblasts, a critical step that has been overlooked previously. Further, they identify a novel regulator of Miranda localization, Kin17, which promotes splicing of the transcript of the PP4 component Falafel.

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Section: Discussionmentioning

confidence: 95%

Kin17 drives dissociation of Mira from the centrosome in neuroblasts by regulating splicing of Flfl

Connell

Xie

Chen

et al. 2021

Preprint

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“…Finally, patients with distant metastasis exhibited higher expression levels of KIN17 than patients without distant metastasis. The TNM staging system is based on the primary tumor, lymph node metastasis and distant metastasis; therefore, the above immunohistochemical results indicate that KIN17 expression is associated with tumor genesis and development (57).…”

Section: Roles Of Kin17 In Cancer Cellsmentioning

confidence: 96%

“…Univariate analysis and Kaplan-Meier survival analysis suggested that KIN17 may serve as a prognostic biomarker for colorectal cancer. In addition to univariate analysis and Kaplan-Meier survival analysis, multivariate Cox regression analysis also indicated that KIN17 was an independent prognostic factor in colorectal cancer (57).…”

Section: Roles Of Kin17 In Cancer Cellsmentioning

confidence: 99%

“…Of note, the DNA damage increased after ultra-violet C radiation or ionizing radiation, resulting in an increase in the expression level of KIN17; in fact, KIN17 gathered in the nucleus forming lesions in cells (13). Furthermore, one study on colorectal cancer revealed that KIN17 is mainly expressed in the nucleus in para-carcinoma tissues, whereas it is expressed both in the nucleus and cytoplasm in the tumor tissues (57). In another study, the components of nuclear and chromatin-related proteins were analyzed, the expression pattern of KIN17 was detected in all components and an increase in the concentration of chromatin-related components of clones with low metastatic potential was observed (58).…”

Section: Kin17 a Dna And Rna Binding Proteinmentioning

confidence: 99%

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Roles and regulatory mechanisms of KIN17 in cancers (Review)

Huang

Dai

et al. 2023

Oncol Lett

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KIN17, which is known as a DNA and RNA binding protein, is highly expressed in numerous types of human cancers and was discovered to participate in several vital cell behaviors, including DNA replication, damage repair, regulation of cell cycle and RNA processing. Furthermore, KIN17 is associated with cancer cell proliferation, migration, invasion and cell cycle regulation by regulating pathways including the p38 MAPK, NF-κB-Snail and TGF-β/Smad2 signaling pathways. In addition, knockdown of KIN17 was found to enhance the sensitivity of tumor cells to chemotherapeutic agents. Immunohistochemical analysis revealed that there were significant differences in the expression of KIN17 between cancer tissues and adjacent tissues. Both the Kaplan-Meier survival analysis and multivariate Cox regression analysis indicated that KIN17 is aberrantly high expressed in various tumor tissues and is also associated with poor prognosis in patients with various tumor types. Taken together, KIN17 has key roles in tumorigenesis and cancer development. Investigating the relationship between KIN17 and neoplasms will provide a vital theoretical basis for KIN17 to serve as a diagnostic and prognostic biomarker for cancer patients and as a potential target for cancer therapy.

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“…Kin17 has reportedly been implicated in DNA replication [10], DNA damage response [11], and cell cycle progression [12] as per earlier investigations. Recent studies have shown that the expression of Kin17 is elevated in a number of tumor types, such as breast cancer [13], colorectal carcinoma [14], hepatocellular carcinoma [15], and non-small cell lung cancer [16]. In cervical cancer samples, there was increased expression of kin17, which is closely correlated with lymph node metastases [17].…”

Section: Introductionmentioning

confidence: 99%

KIN17 modulates cell proliferation and migration through the WNT/β-catenin signal pathways in non-small cell lung cancer

Peng

Wei

Lin

et al. 2023

Preprint

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Background KIN17 DNA and RNA binding protein (KIN17) regulates the tumorigenesis of a variety of human cancers. Non-small cell lung cancer’s (NSCLC) molecular mechanisms for cancer metastasis and growth, however, are still unknown. Methods KIN17’s expression pattern as well as its prognostic value in LUAD patients was examined utilizing bioinformatics, and KIN17 co-expression network was enriched by the KEGG pathway and built via protein-protein interaction (PPI) network. Western blotting and Real-time quantitative PCR were employed to find Kin17 expression in NSCLC cells. Moreover, total amounts of EMT, WNT-related proteins, and β-catenin were also found using Western blotting. The expression of N‑cadherin, E-cadherin, and Vimentin was examined using immunohistochemical and immunofluorescent staining. The invasive and proliferative capacities of cancer cells were examined in vitro using wound healing, proliferation, cell cycle, transwell migration, and apoptosis. The impacts of KIN17 on the invasive and proliferative capacities in vivo were studied using the tumor xenograft model. Results On the basis of the TIMRE database, the mRNA expression of KIN was shown to be considerably higher in tumor tissues in contrast to adjacent normal tissues, and the protein expression of KIN was found to be considerably higher in LUAD from the National Cancer Institute. Then, in the LUAD from the TCGA database, patients with increased KIN17 expression had lowest disease free survival (DFS). The co-expression network of KIN17 enriched pathways were obtained by KEGG enrichment analysis and found to be linked to the tumorigenesis and development, including tight junction, WNT signaling pathway, regulation of actin cytoskeleton, and focal adhesion. In NSCLC cells, KIN17 was also upregulated in H1299 cell. With an increased expression of E-cadherin and a reduced expression of Vimentin and N-cadherin, KIN17 knockdown in H1299 cells greatly inhibited the ability of cells to invade, proliferate, and migrate. KIN17 knockdown likewise impaired WNT/β-catenin signal pathways, as indicated by downregulated expression of the WNT and β-catenin in vitro. Furthermore, KIN17 knockdown significantly reduced tumor renewal in NSCLC xenograft models. Conclusions By blocking the WNT/β-catenin pathway, KIN17 knockdown prevents EMT, NSCLC proliferation, and invasion.

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Relationships of kin17 protein expression with clinical features and prognosis of colorectal cancer

Abstract: Background: To investigate the relationships of kin17 protein expression with the clinical features and prognosis of colorectal cancer (CRC). Methods:The clinicopathological data and paraffin specimens of 135 CRC patients in the First

Cited by 4 publications

References 14 publications

Kin17 drives dissociation of Mira from the centrosome in neuroblasts by regulating splicing of Flfl

Kin17 drives dissociation of Mira from the centrosome in neuroblasts by regulating splicing of Flfl

Roles and regulatory mechanisms of KIN17 in cancers (Review)

KIN17 modulates cell proliferation and migration through the WNT/β-catenin signal pathways in non-small cell lung cancer

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