Expression of Kin17 promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo

Kou, Weizheng; Xu, Suling; Wang, Ying; Wang, Li‐Wei; Wang, Lei; Chai, Xiaoyan; Qin-liang, Hua

doi:10.3892/ol.2014.2244

Cited by 14 publications

(17 citation statements)

References 19 publications

(24 reference statements)

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“…To investigate the potential targets for TNBC, the role of kin17 in a TNBC cell line was investigated. Kin17, a constitutive gene with extremely low expression in the majority of human tissues, has been reported to be markedly overexpressed in multiple tumors including breast cancer (10–13). In the present study, a lentiviral vector was used to stably knockdown kin17.…”

Section: Discussionmentioning

confidence: 99%

“…Studies have shown that kin17 is closely correlated with DNA replication, mRNA processing and cell cycle regulation (8,9). Kin17 was previously revealed to be upregulated in various tumors, including breast cancer, colorectal carcinoma, hepatocellular carcinoma and non-small cell lung cancer (10–13). Specifically, Zeng et al (10) demonstrated that kin17 is essential for the proliferation of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

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Knockdown of DNA/RNA‑binding protein KIN17 promotes apoptosis of triple‑negative breast cancer cells

Gao

Liu²,

Zhong

et al. 2018

Oncol Lett

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Effective therapy for breast cancer has been extensively studied worldwide, particularly for triple-negative breast cancer and drug-resistant subtypes. DNA/RNA-binding protein KIN17 (kin17) has been reported to be significantly upregulated in breast cancer cells, and is proposed to serve a role in the regulation of cell proliferation. The present study further investigated the association of kin17-knockdown with breast cancer cell apoptosis. Cell Counting kit-8, flow cytometry, TUNEL assay and caspase 3/7 analysis were performed on MDA-MB-231 cells to determine the association between kin17 and breast cancer cell apoptosis. In addition, western blot analysis was performed to investigate the mechanism of kin17 in the apoptosis of MDA-MB-231 cells. The results revealed that knockdown of kin17 inhibited proliferation and promoted apoptosis of MDA-MB-231 cells, and suggested a poly (adenosine diphosphate-ribose) polymerase-related mechanism behind the apoptosis of the cells. These findings suggested that kin17 could become a novel target for breast cancer therapy.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Knockdown of DNA/RNA‑binding protein KIN17 promotes apoptosis of triple‑negative breast cancer cells

Gao

Liu²,

Zhong

et al. 2018

Oncol Lett

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“…At present, the expression level of KIN17 in human tumors remains unclear. Recently, studies performed by Yu et al ( 10 ) and Kou et al ( 9 ) revealed that KIN17 gene expression is upregulated in colorectal cancer and hepatocellular carcinoma, respectively. In addition, a previous study demonstrated that KIN17 was markedly overexpressed in breast cancer ( 8 ).…”

Section: Discussionmentioning

confidence: 99%

“…Following purification and titration, the harvested virus particles were used to infect the A549 cells as described by Kou ( 9 ). KIN17 mRNA levels in total RNA extracted from the infected cells was determined through RT-qPCR as described above.…”

Section: Methodsmentioning

confidence: 99%

Upregulation of KIN17 is associated with non-small cell lung cancer invasiveness

et al. 2017

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Kin17 DNA and RNA binding protein (Kin17) is a highly conserved protein that participates in DNA replication, DNA repair and cell cycle progression. Recently, the tumor-promoting function of Kin17 has been demonstrated and increasingly studied. In the present study, the role of Kin17 in the invasion and metastasis of non-small cells lung cancer (NSCLC) was investigated. Elevated Kin17 mRNA and protein expression was identified in a total of 97 NSCLC and benign lung lesion tissue specimens. Kin17 overexpression was significantly correlated with high tumor grade and lymph node metastasis, indicating poor patient prognosis. Scratch and Transwell assays demonstrated that the knockdown of KIN17 inhibited the ability of NSCLC cells to migrate and invade. Furthermore, reverse transcription-quantitative polymerase chain reaction and western blot analyses confirmed that knockdown of KIN17 decreased the expression of matrix metalloproteinase 7, epidermal growth factor receptor and v-myc avian myelocytomatosis viral oncogene homolog. The results of the present study indicate that Kin17 is markedly overexpressed in NSCLC tissues compared with benign lung lesion and peritumoral tissue. The upregulation of KIN17 may serve an important role in the metastasis of NSCLC cells. These results indicate that Kin17 is a novel diagnostic and prognostic biomarker of NSCLC, in addition to being a potential therapeutic target for the treatment of patients with NSCLC.

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“…Proliferation, invasion and metastasis are inhibited by downregulation of the KIN17 protein, thereby inducing apoptosis and cell cycle arrest in cervical cancer cells ( 17 ). The KIN17 protein can induce the proliferation of liver cancer cells ( 18 ), and its upregulation is associated with the invasion and metastasis of non-small cell lung cancer ( 19 ). However, to the best of our knowledge, the effect of KIN17 in ovarian cancer remains unclear and requires further exploration.…”

Section: Introductionmentioning

confidence: 99%

Analysis of the association between KIN17 expression and the clinical features/prognosis of epithelial ovarian cancer, and the effects of KIN17 in SKOV3 cells

et al. 2021

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DNA double-strand breaks (DSBs) are an important mechanism of chemotherapy in epithelial ovarian cancer (EOC). Kin17 DNA and RNA binding protein (KIN17) serves a crucial role in DSB repair. In the present study, the association between KIN17 and EOC, and the effects of KIN17 on EOC cells in vitro were evaluated. A bioinformatics method was used to determine the mRNA expression levels of KIN17 in EOC and its association with EOC prognosis including overall survival (OS) and progression free survival (PFS) time. Western blotting and immunohistochemical staining were used to evaluate the expression levels of KIN17 in EOC samples. Kaplan-Meier and Cox regression analyses were utilized to analyze risk factors for the OS of patients with EOC. A Cell Counting Kit-8 assay was performed to explore the roles of KIN17 in SKOV3 cells. Both the transcription and expression of KIN17 were upregulated in EOC tissues. Furthermore, the OS of patients with EOC with high mRNA expression levels of KIN17 was shorter than that of patients with EOC with low expression levels. High KIN17 expression was an independent risk factor for EOC prognosis. Furthermore, KIN17 knockdown inhibited the proliferation of SKOV3 cells, enhanced the sensitivity of the cells to cisplatin and inhibited the migration ability of the cells. These results suggested that KIN17 may act as an ideal candidate for therapy and as a prognostic biomarker of EOC, although the underlying mechanisms require further exploration.

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Expression of Kin17 promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo

Cited by 14 publications

References 19 publications

Knockdown of DNA/RNA‑binding protein KIN17 promotes apoptosis of triple‑negative breast cancer cells

Knockdown of DNA/RNA‑binding protein KIN17 promotes apoptosis of triple‑negative breast cancer cells

Upregulation of KIN17 is associated with non-small cell lung cancer invasiveness

Analysis of the association between KIN17 expression and the clinical features/prognosis of epithelial ovarian cancer, and the effects of KIN17 in SKOV3 cells

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