ZNF367-induced transcriptional activation of KIF15 accelerates the progression of breast cancer

Zeng, Huijuan; Li, Tianfu; Zhai, Duanyang; Bi, Jiong; Kuang, Xiaying; Lu, Si-Hong; Zhang, Shan; Lin, Ying

doi:10.7150/ijbs.44204

Cited by 19 publications

(16 citation statements)

References 23 publications

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“…The protein expression of KIF15 in NPC tissues was signi cantly higher than para-carcinoma tissues, which was signi cantly correlated with cancer grades, recurrence and predicted a poor prognosis of patients. Similar results have also been reported in hepatocellular carcinoma [10], lung cancer [12], breast cancer [22] and other tumors [13,23]. All these indicate that the high expression of KIF15 is an unfavorable factor for the prognosis of tumor patients.…”

Section: Discussionsupporting

confidence: 84%

KIF15 Accelerated The Progression of Nasopharyngeal Carcinoma and Predict Poor Prognosis

Wang¹,

Yong²,

Qin³

et al. 2021

Preprint

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Background: Nasopharyngeal carcinoma (NPC) is a common tumor in head and neck and is prevailing in China. Although treatment methods continue to improve, the prognosis of advanced patients is still unsatisfactory. Kinesin family member 15 (KIF15) is a kind of protein, which regulates the process of cell mitosis and plays an important role in several types of human cancers. This study aims to investigate the role of KIF15 in NPC.Methods: First, the differential expression of KIF15 in NPC and para-carcinoma tissues was evaluated based on both data collected from Gene Expression Omnibus (GEO) database and immunohistochemical analysis on clinical specimens collected from in-house cohort. Next, cell lines C666-1 and CNE-2Z were selected for the construction of KIF15‑knockdown cell models. Then, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, flow cytometry, wound healing, Transwell and clone formation assays were used to detect the proliferation, apoptosis, migration, invasion and colony formation of nasopharyngeal carcinoma cells in vitro. A mouse xenograft model was constructed for in vivo study. Furthermore, Human Apoptosis Antibody Array kit was used to screen possible targets of KIF15 in NPC. In the end, the potential molecular mechanisms underlying the effects of KIF15 was explored through western blot analysis.Results: The results showed that the expression of KIF15 in NPC tissues is higher than that in para-carcinoma tissues, and high levels of KIF15 expression are associated with low survival rates. In addition, knockdown of KIF15 inhibited cell proliferation, migration, invasion and colony formation ability, and promoted cell apoptosis. What’s more, in vivo xenograft experiments showed that down-regulation of KIF15 can inhibit NPC tumor growth. Moreover, the mechanism study demonstrated a variety of apoptosis-related proteins as well as PI3K/AKT and MAPK signaling pathways may be involved in KIF15-induced regulation of NPC.Conclusions: In short, we demonstrated that KIF15 is overexpressed and accelerated the progression of nasopharyngeal carcinoma. It can be used as a new prognostic indicator as well as a potential drug target for the treatment of NPC.

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Section: Discussionsupporting

confidence: 84%

KIF15 Accelerated The Progression of Nasopharyngeal Carcinoma and Predict Poor Prognosis

Wang¹,

Yong²,

Qin³

et al. 2021

Preprint

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“…39 ZNF367 has been reported has a key controller of the neuroblast cell cycle, 40 and it has been reported to accelerate cell cycle progression in breast cancer. 35 Importantly, our rescue experiments confirmed that downregulation of miR-330 in U251 and SHG44 cells restored the levels of PCNA, CDC20, CDC7 and CCNA1, indicating that the GABPB1-AS1/miR-330/ZNF367 axis regulates the cell cycle signaling pathway to govern the malignant behaviors of glioma cells.…”

Section: Discussionsupporting

confidence: 60%

“…Next, ZNF367 was confirmed as a target of miR-330 and was highly expressed in glioma tissues. As a member of the zinc finger transcription factor family, ZNF367 has been reported to accelerate metastasis and progression of breast cancer 34,35 and pancreatic cancer. 36 Here, the subsequent KEGG pathway enrichment analysis suggested that the ZNF367-related genes were enriched on the cell cycle signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA GABPB1-AS1 Augments Malignancy of Glioma Cells by Sequestering MicroRNA-330 and Reinforcing the ZNF367/Cell Cycle Signaling Pathway

Li¹,

Wang²

2021

NDT

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Background: Deregulation of long non-coding RNAs (lncRNAs) is frequently relevant to the malignant phenotypical changes. This study aimed to explore the role of lncRNA GABPB1-AS1 in the malignancy of glioma cells. Methods: Abnormally expressed genes in glioma were analyzed using a GEO GSE2223 dataset. Short hairpin (sh) RNA silencing of GABPB1-AS1 was introduced in glioma cells to explore its correlation with the proliferation, apoptosis, and invasiveness of cancer cells. The target transcripts of GABPB1-AS1 were predicted by bioinformatics analyses. MicroRNA (miR)-330 inhibition was additionally introduced in the glioma cells after GABPB1-AS1 knockdown for rescue experiments. Animal studies were performed by inducing xenograft tumors in nude mice. Results: GABPB1-AS1 was highly expressed in the glioma tissues and associated with advanced WHO grades. GABPB1-AS1 knockdown reduced proliferation and invasiveness of glioma cells in vitro and in vivo. miR-330 was a target transcript of GABPB1-AS1. miR-330 inhibition restored the malignancy of glioma cells. miR-330 directly bound to ZNF367. ZNF367 was highly expressed in glioma tissues and positively correlated with GABPB1-AS1 expression, and it was relevant to the cell cycle signaling pathway. Downregulation of GABPB1-AS1 reduced the expression of ZNF367 and reduced the levels of cell cycle-related proteins PCNA, CDC20, CDC7 and CCNA1 in cells. Conclusion:This study demonstrated that GABPB1-AS1 competitively bound to miR-330 and de-repressed ZNF367 expression, leading to activation of the cell cycle signaling pathway and the growth and metastasis of glioma cells.

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“…The flowchart of literature retrieval process is shown in Supplementary Figure 1. The basic characteristics of all included studies (12,14,(19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29) or datasets are shown in Supplementary Table 2 and Supplementary Table 3.…”

Section: Correlation Analysis Between the Expression Of Kif15 And Pro...mentioning

confidence: 99%

Integrative Pan-Cancer Analysis of KIF15 Reveals Its Diagnosis and Prognosis Value in Nasopharyngeal Carcinoma

Chen

et al. 2022

Front. Oncol.

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BackgroundKIF15 plays a vital role in many biological processes and has been reported to influence the occurrence and development of certain human cancers. However, there are few systematic evaluations on the role of KIF15 in human cancers, and the role of KIF15 in the diagnosis and prognosis of nasopharyngeal carcinoma (NPC) also remains unexplored. Therefore, this study aimed to conduct a pan-cancer analysis of KIF15 and evaluate its diagnostic and prognostic potential in NPC.MethodsThe expression pattern, prognostic value, molecular function, tumor mutation burden, microsatellite instability, and immune cell infiltration of KIF15 were examined based on public databases. Next, the diagnostic value of KIF15 in NPC was analyzed using the Gene Expression Omnibus (GEO) database and immunohistochemistry (IHC). Kaplan–Meier curves, Cox regression analyses, and nomograms were used to evaluate the effects of KIF15 expression on NPC prognosis. Finally, the effect of KIF15 on NPC was explored by in vitro experiments.ResultsThe expression of KIF15 was significantly upregulated in 20 out of 33 cancer types compared to adjacent normal tissue. Kyoto Encyclopedia of Genes and Genomes enrichment (KEGG) analysis showed that KIF15 could participate in several cancer-related pathways. The increased expression level of KIF15 was correlated with worse clinical outcomes in many types of human cancers. Additionally, KIF15 expression was related to cancer infiltration of immune cells, tumor mutation burden, and microsatellite instability. In the analysis of NPC, KIF15 was significantly upregulated based on the GEO database and immunohistochemistry. A high expression of KIF15 was negatively associated with the prognosis of patients with NPC. A nomogram model integrating clinical characteristics and KIF15 expression was established, and it showed good predictive ability with an area under the curve value of 0.73. KIF15 knockdown significantly inhibited NPC cell proliferation and migration.ConclusionsOur findings revealed the important and functional role of KIF15 as an oncogene in pan-cancer. Moreover, high expression of KIF15 was found in NPC tissues, and was correlated with poor prognosis in NPC. KIF15 may serve as a potential therapeutic target in NPC treatment.

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ZNF367-induced transcriptional activation of KIF15 accelerates the progression of breast cancer

Cited by 19 publications

References 23 publications

KIF15 Accelerated The Progression of Nasopharyngeal Carcinoma and Predict Poor Prognosis

KIF15 Accelerated The Progression of Nasopharyngeal Carcinoma and Predict Poor Prognosis

Long Non-Coding RNA GABPB1-AS1 Augments Malignancy of Glioma Cells by Sequestering MicroRNA-330 and Reinforcing the ZNF367/Cell Cycle Signaling Pathway

Integrative Pan-Cancer Analysis of KIF15 Reveals Its Diagnosis and Prognosis Value in Nasopharyngeal Carcinoma

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