Knockdown of Kif20a inhibits growth of tumors in soft tissue sarcoma in vitro and in vivo

Zhu, Zhifeng; Jin, Zheng; Zhang, Haibo; Zhang, Mei; Sun, Dahui

doi:10.7150/jca.44777

Cited by 9 publications

(7 citation statements)

References 23 publications

(25 reference statements)

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“…KIF20A can affect the prognosis of bladder cancer by promoting the proliferation and metastasis of bladder cancer cells.KIF20A [ 22 ]. In soft tissue sarcoma, KIF20A gene knockout can inhibit the proliferation, migration and invasion of soft tissue sarcoma cells, promote cell apoptosis, and inhibit tumor growth [ 23 ]. These results indicated that KIF20A had an important effect on the proliferation, invasion and apoptosis of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of KIF20A by transcription factor IRF6 affects the progression of renal clear cell carcinoma

Wang

Dong

et al. 2021

Cancer Cell Int

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Background Renal clear cell carcinoma (ccRCC) is one of the most common malignant tumors, whose incidence is increasing year by year. IRF6 plays an important role in the occurrence of tumors, although there is yet no report on its expression in ccRCC. Methods The expression of IRF6 and KIF20A in ccRCC was predicted by GEPIA and HAP databases. In addition, GEPIA database predicted the relationship between IRF6 and KIF20A expressions and the pathological staging, overall survival, and disease-free survival of ccRCC. The possible binding sites of IRF6 and KIF20A promoters were predicted by JASPAR database and verified by luciferase and ChIP assays. The specific effects of IRF6 on ccRCC cell proliferation, invasion and apoptosis were subsequently examined at both cellular level and animal level. Results The database predicted down-regulated IRF6 expression in renal carcinoma tissues and its correlation with poor prognosis. IRF6 overexpression inhibited cRCC cell proliferation, invasion and migration. In addition, up-regulated KIF20A expression in renal carcinoma tissues and its association with prognosis were also predicted. Interference with KIF20A inhibited the proliferation, invasion, and migration of ccRCC cells. Finally, we confirmed that KIF20A is a functional target of IRF6 and can partially reverse the effects of IRF6 on the proliferation, invasion and migration of ccRCC cells. Conclusion: Inhibition of KIF20A by transcription factor IRF6 affects cell proliferation, invasion and migration in renal clear cell carcinoma.

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Section: Discussionmentioning

confidence: 99%

Inhibition of KIF20A by transcription factor IRF6 affects the progression of renal clear cell carcinoma

Wang

Dong

et al. 2021

Cancer Cell Int

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“…MCA‐induced fibrosarcoma 207 is a well‐established soft tissue sarcoma model that is used to study tumour regression and immunity in C57BL/6 mice. 11 , 12 [ S3 ] Continuous passaging of MCA207 cells caused a ‘drift’ in tumour phenotype and cachexia in CHX207‐tumour‐bearing mice. Intramuscular injection of MCA207‐ or CHX207 cells resulted in solid tumours, which were palpable around 7 days post injection (p.i.).…”

Section: Resultsmentioning

confidence: 99%

Interleukin‐6 initiates muscle‐ and adipose tissue wasting in a novel C57BL/6 model of cancer‐associated cachexia

Pototschnig

Feiler

Vesely

et al. 2022

J cachexia sarcopenia muscle

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Background Cancer‐associated cachexia (CAC) is a wasting syndrome drastically reducing efficacy of chemotherapy and life expectancy of patients. CAC affects up to 80% of cancer patients, yet the mechanisms underlying the disease are not well understood and no approved disease‐specific medication exists. As a multiorgan disorder, CAC can only be studied on an organismal level. To cover the diverse aetiologies of CAC, researchers rely on the availability of a multifaceted pool of cancer models with varying degrees of cachexia symptoms. So far, no tumour model syngeneic to C57BL/6 mice exists that allows direct comparison between cachexigenic‐ and non‐cachexigenic tumours. Methods MCA207 and CHX207 fibrosarcoma cells were intramuscularly implanted into male or female, 10–11‐week‐old C57BL/6J mice. Tumour tissues were subjected to magnetic resonance imaging, immunohistochemical‐, and transcriptomic analysis. Mice were analysed for tumour growth, body weight and ‐composition, food‐ and water intake, locomotor activity, O2 consumption, CO2 production, circulating blood cells, metabolites, and tumourkines. Mice were sacrificed with same tumour weights in all groups. Adipose tissues were examined using high‐resolution respirometry, lipolysis measurements in vitro and ex vivo, and radioactive tracer studies in vivo. Gene expression was determined in adipose‐ and muscle tissues by quantitative PCR and Western blotting analyses. Muscles and cultured myotubes were analysed histologically and by immunofluorescence microscopy for myofibre cross sectional area and myofibre diameter, respectively. Interleukin‐6 (Il‐6) was deleted from cancer cells using CRISPR/Cas9 mediated gene editing. Results CHX207, but not MCA207‐tumour‐bearing mice exhibited major clinical features of CAC, including systemic inflammation, increased plasma IL‐6 concentrations (190 pg/mL, P ≤ 0.0001), increased energy expenditure (+28%, P ≤ 0.01), adipose tissue loss (−47%, P ≤ 0.0001), skeletal muscle wasting (−18%, P ≤ 0.001), and body weight reduction (−13%, P ≤ 0.01) 13 days after cancer cell inoculation. Adipose tissue loss resulted from reduced lipid uptake and ‐synthesis combined with increased lipolysis but was not associated with elevated beta‐adrenergic signalling or adipose tissue browning. Muscle atrophy was evident by reduced myofibre cross sectional area (−21.8%, P ≤ 0.001), increased catabolic‐ and reduced anabolic signalling. Deletion of IL‐6 from CHX207 cancer cells completely protected CHX207IL6KO‐tumour‐bearing mice from CAC. Conclusions In this study, we present CHX207 fibrosarcoma cells as a novel tool to investigate the mediators and metabolic consequences of CAC in C57BL/6 mice in comparison to non‐cachectic MCA207‐tumour‐bearing mice. IL‐6 represents an essential trigger for CAC development in CHX207‐tumour‐bearing mice.

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“…The overexpression of KIF20A is linked to the onset, progression, and prognosis of different cancers. Recent researches have reported that KIF20A was upregulated in esophageal squamous cell carcinoma ( 28 ), lung adenocarcinoma ( 29 ), prostate cancer ( 30 ), cervical cancer ( 31 ), colorectal cancer ( 32 ), non-small cell lung cancer ( 33 ), gastric cancer ( 34 ), bladder cancer ( 35 ), renal clear cell carcinoma ( 36 ), breast cancer ( 37 ), hepatocellular carcinoma ( 38 ), nasopharyngeal carcinoma ( 39 ), ovarian cancer ( 40 ), leukemia ( 25 ), glioma ( 41 ), and soft tissue sarcoma ( 42 ). This is consistent with our analysis in the GEPIA online database.…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Transcriptome Data Revealed AURKA and KIF20A as Critical Genes in Medulloblastoma Progression

et al. 2022

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Medulloblastoma is the neuroepithelial tumor with the highest degree of malignancy in the central nervous system, accounting for about 8% to 10% of children’s brain tumors. It has a high degree of malignancy and is easily transmitted through cerebrospinal fluid, with a relatively poor prognosis. Although medulloblastoma has been widely studied and treated, its molecular mechanism remains unclear. To determine which gene plays a crucial role in medulloblastoma development and progression, we analyzed three microarray datasets from Gene Expression Omnibus. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were used to detect and evaluate differentially expressed genes. Protein interaction network was established, and the hub genes were determined in cytoHubba through various assessment methods, while the target genes were screened out using survival analysis. Ultimately, human medulloblastoma samples were utilized to confirm target gene expression. In conclusion, This study found that aurora kinase A (AURKA) and kinesin family member 20A (KIF20A) may be involved in the initiation and development of medulloblastoma, have a close association with prognosis, and may become a potential therapeutic target and prognostic marker of MED.

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Knockdown of Kif20a inhibits growth of tumors in soft tissue sarcoma in vitro and in vivo

Cited by 9 publications

References 23 publications

Inhibition of KIF20A by transcription factor IRF6 affects the progression of renal clear cell carcinoma

Inhibition of KIF20A by transcription factor IRF6 affects the progression of renal clear cell carcinoma

Interleukin‐6 initiates muscle‐ and adipose tissue wasting in a novel C57BL/6 model of cancer‐associated cachexia

Integrated Analysis of Transcriptome Data Revealed AURKA and KIF20A as Critical Genes in Medulloblastoma Progression

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