Elevated MYO10 Predicts Poor Prognosis and its Deletion Hampers Proliferation and Migration Potentials of Cells Through Rewiring PI3K/Akt Signaling in Cervical Cancer

He, Jiaxun; Chen, Jianguo; Zhang, Bin; Chen, Jing; You, Keli; Hu, Jie-Mei; Xu, Jiawen; Chen, Le

doi:10.1177/1533033820936773

Cited by 6 publications

(6 citation statements)

References 32 publications

(39 reference statements)

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“…Furthermore, studies on survivals revealed that patients with a high MYO10 expression had a worse chance to survive the disease overall. In addition, by rewiring the PI3K/Akt signaling pathway of CC caused by the knockdown or overexpression of MYO10, the capability of cervical cells in terms of proliferation, invasion, and migration was dramatically hindered or improved [ 31 ]. These findings showed that some tumor-related genes might have the potential to be employed as new biomarkers for the diagnosis and prognosis of individuals suffering from CC.…”

Section: Discussionmentioning

confidence: 99%

Integrated Analyses of the Expression and Prognostic Value of EPHB6 in Cervical Cancer and Its Correlation with Immune Infiltrates

Xiang

Wei

Zhao

et al. 2023

Journal of Oncology

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Among women, cervical cancer (CC) ranks as the third most frequent form of carcinoma and the fourth greatest cancer-related cause of deaths. There is increasing evidence that points to the dysregulation of EPH receptor B6 (EPHB6) in various cancers. On the other hand, neither the expression nor the function of EPHB6 in CC has been researched. In the first part of this investigation, we analyzed the data from the TCGA and discovered that the level of EPHB6 was much lower in CC tissues than in normal cervical tissues. ROC assays revealed that high EPHB6 expression had an AUC value of 0.835 for CC. The survival study revealed that both the overall and disease-specific survivals in this condition were considerably lower among patients who had a low EPHB6 level compared to those who had a high EPHB6 level. It is important to note that the multivariate COX regression analysis indicated that the expression of EPHB6 was an independent predictive factor. In addition to this, the C-indexes and calibration plots of a nomogram derived from multivariate assays revealed an accurate prediction performance among patients with CC. Immune infiltration analysis indicated that the expression of EPHB6 was positively associated with the levels of Tcm, TReg, B cells, T cells, iDC, T helper cells, cytotoxic cells, and DC, while negatively associated with NK CD56bright cells and neutrophils. In summary, the downregulation of EPHB6 was strongly linked to a more aggressive clinical development of CC, suggesting its potential utility as a diagnostic and therapeutic target in CC.

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Section: Discussionmentioning

confidence: 99%

Integrated Analyses of the Expression and Prognostic Value of EPHB6 in Cervical Cancer and Its Correlation with Immune Infiltrates

Xiang

Wei

Zhao

et al. 2023

Journal of Oncology

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“…MYO10 is highly expressed in several types of cancer, and increased MYO10 promotes breast cancer invasion and metastasis 10,11 . Moreover, elevated MYO10 predicts poor prognosis and promotes cell proliferation and migration in cervical cancer 14 36 .…”

Section: Discussionmentioning

confidence: 99%

“… 10 , 11 Moreover, elevated MYO10 predicts poor prognosis and promotes cell proliferation and migration in cervical cancer. 14 Some researchers found that MYO10‐driven filopodia are crucial for leader driven NSCLC collective invasion. 36 Recently, it has been demonstrated that MYO10 drives genomic instability and inflammation in cancer.…”

Section: Discussionmentioning

confidence: 99%

“…MYO10 is broadly distributed in many tissues 4 and involved in numerous essential biological process, for example, orientation of the mitotic spindle, 5 endothelial cell migration and angiogenesis, 6 filopodia formation, 7 and cell motility. 8 In addition, numerous studies have found that MYO10 is highly expressed in melanoma, 9 breast cancer, 10 , 11 non–small cell lung cancer, 12 prostate cancer, 13 and cervical cancer, 14 compared with normal tissues, and promotes proliferation, invasion, and migration of tumor cells. However, its functional role in metastasis, especially in liver metastasis, has yet to be fully characterized.…”

Section: Introductionmentioning

confidence: 99%

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MYO10 contributes to the malignant phenotypes of colorectal cancer via RACK1 by activating integrin/Src/FAK signaling

Wang

et al. 2022

Cancer Science

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Liver metastases still remain a major cause of colorectal cancer (CRC) patient death. MYO10 is upregulated in several tumor types; however, its significance and the underlying mechanism in CRC are not entirely clear. Here, we found that MYO10 was highly expressed in CRC tumor tissues, especially in liver metastasis tissues. MYO10 knockout reduced CRC cell proliferation, invasion, and migration in vitro and CRC metastasis in vivo. We identified RACK1 by LC‐MS/MS and demonstrated that MYO10 interacts with and stabilizes RACK1. Mechanistically, MYO10 promotes CRC cell progression and metastasis via ubiquitination‐mediated RACK1 degradation and integrin/Src/FAK signaling activation. Therefore, the MYO10/RACK1/integrin/Src/FAK axis may play an important role in CRC progression and metastasis.

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“…However, abnormalities in the fused eyelids and fingers, larynx and vagina are caused by failed programmed cell death [ 11 , 12 ]. The MYO10 gene plays a certain role in limb development and promotes cell migration in vivo and in vitro [ 13 , 14 ]. The six candidate genes obtained by second-generation sequencing in this study were analysed by Sanger sequencing and other methods.…”

Section: Discussionmentioning

confidence: 99%

Identification of a HOXD13 variant in a Mongolian family with incomplete penetrance syndactyly by exon sequencing

Husile¹,

Wu²,

Yang³

et al. 2022

BMC Med Genomics

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Background Syndactyly (SD) refers to a deformity caused by the fusion and limb differentiation disorder of soft tissues and/or skeletons to varying extents between adjacent fingers (toes). The main features of this disease are phenotypic heterogeneity and genetic heterogeneity. In this study, we examined four generations of a Chinese Mongolian with different phenotypes of syndactylia and analysed and identified the pathogenic genetic variants of SD by exon sequencing. Methods The clinical phenotypes of patients were analysed, and the hands and feet were examined by X-ray. The pedigree was drawn, and the family data were analysed. Peripheral blood was collected from the family members, and genomic DNA was extracted. The candidate genes of SD were identified by exon sequencing, and the mutation sites of the captured candidate genes were amplified by PCR and verified by Sanger sequencing. Results The family has congenital syndactyly, which is an autosomal dominant disease. At present, this condition has been passed down for 4 generations and was identified in 9 patients, including 4 males and 5 females. Five patients, I2, II4, III5, III,7 and III10, had unilateral syndactyly, and four patients, III16, IV3, IV6 and IV7, had bilateral finger syndactyly. All of their toes were unaffected. The proband and the other patients in this family had a c.917G > A (p.R306Q) mutation, which is located at position 917 of the second exon of the HOXD13 gene. This mutation results in a change in the amino acid at position 306, in which arginine is changed to glutamine. This mutation cosegregates in unaffected individuals and affected patients in this family. Moreover, 201 Mongolian genome databases and a thousand human genome databases were referenced to further confirm that the pathogenic genetic variant that causes syndactyly in this family is found in HOXD13. Conclusion This study found that the mutation site of the pathogenic gene in this family was HOXD13, c.917G > A (p.R306Q). The phenotype of the family member III12 was normal, but this member was also a carrier of the pathogenic genetic variant. This indicates that the disease of this family has incomplete penetrance characteristics. Our results further enrich the expression profile of the HOXD13 gene.

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Elevated MYO10 Predicts Poor Prognosis and its Deletion Hampers Proliferation and Migration Potentials of Cells Through Rewiring PI3K/Akt Signaling in Cervical Cancer

Cited by 6 publications

References 32 publications

Integrated Analyses of the Expression and Prognostic Value of EPHB6 in Cervical Cancer and Its Correlation with Immune Infiltrates

Integrated Analyses of the Expression and Prognostic Value of EPHB6 in Cervical Cancer and Its Correlation with Immune Infiltrates

MYO10 contributes to the malignant phenotypes of colorectal cancer via RACK1 by activating integrin/Src/FAK signaling

Identification of a HOXD13 variant in a Mongolian family with incomplete penetrance syndactyly by exon sequencing

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