Overexpression of PTK6 predicts poor prognosis in bladder cancer patients

Xu, Xue Lian; Ye, Yun Lin; Wu, Zhiyuan; He, Qiu; Tan, Liang; Xiao, Kang; Wu, Rui; Yu, Yan; Mai, Jia; Li, Zhi Ling; Peng, Xiao; Huang, Yun; Liu, Xuan; Zhang, Hai Liang; Zhu, Xiao Feng; Qin, Zi Ke

doi:10.7150/jca.21318

Cited by 23 publications

(21 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…38 PTK6 overexpression strongly correlated to the grade, recurrence as well as poor prognosis of bladder cancer patients, and PTK6 knockdown contributed to considerably suppressed cell proliferation and migration. 39 Meanwhile, the oncogenic role of PTK6 was also revealed by Wozniak et al in prostate cancer. 40 Furthermore, sustained induction of the JAK2/STAT3 pathway is highly correlated to tumorigenesis, proliferation, apoptosis and metastasis of tumors, including CC.…”

Section: Discussionmentioning

confidence: 89%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

View full text Add to dashboard Cite

Serum response factor (SRF), a sequence-specific transcription factor, is closely related to metastasis of gastric cancer, a digestive tract cancer. Herein, we probed the effect of SRF on metastasis and progression of colon cancer (CC), another digestive tract disorder, and the detailed mechanism. Methods: Microarray analysis was conducted on tumor and adjacent tissues to filter differentially expressed miRNA, followed by RT-qPCR validation in CC cell lines. The transcription factor and the target gene of microRNA-214 (miR-214) were predicted, and their binding relationships were tested by luciferase reporter assays and ChIP assays. Subsequently, SRF and protein tyrosine kinase 6 (PTK6) expression in CC patients and cells was evaluated by RT-qPCR, while JAK2 and STAT3 expression in cells by Western blot analysis. To further explore functions of miR-214, PTK6 and SRF on CC, CC cells were delivered with si-PTK6, miR-214 mimic and/or SRF overexpression. Results: miR-214 expressed poorly in CC tissues and cell lines, which related to advanced TNM staging and survival. miR-214 mimic inhibited proliferation, migration, invasion, xenograft tumor growth and metastasis of CC cells. SRF, overexpressed in CC samples and cells, suppressed the transcription of miR-214. Meanwhile, SRF upregulation counteracted the inhibitory role of miR-214 mimic in CC cell growth. miR-214 negatively regulated PTK6 expression to impair the JAK2/STAT3 pathway activation, thereby halting CC cell proliferation, migration, invasion, xenograft tumor growth and metastasis. Conclusion: Altogether, miR-214 may perform as a tumor suppressor in CC, and the SRF/ miR-214/PTK6/JAK2/STAT3 axis could be applied as a biomarker and potential therapeutic target.

show abstract

Section: Discussionmentioning

confidence: 89%

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

Li¹,

Wan²,

Su³

et al. 2020

CMAR

View full text Add to dashboard Cite

show abstract

“…PTK6 is known to regulate cell survival, differentiation, and metastasis. Increased expression and an oncogenic role of PTK6 has been shown in multiple cancers including PCa 33,34,57,58 . In PCa, PTK6 overexpression is associated with cell growth, metastasis, and poor prognosis 33,39,41,59 .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells

Cagle

Niture

Srivastava

et al. 2019

Sci Rep

View full text Add to dashboard Cite

Prostate cancer is the most commonly diagnosed cancer in men with African American men disproportionally suffering from the burden of this disease. Biomarkers that could discriminate indolent from aggressive and drug resistance disease are lacking. MicroRNAs are small non-coding RNAs that affect numerous physiological and pathological processes, including cancer development and have been suggested as biomarkers and therapeutic targets. In the present study, we investigated the role of miR-214 on prostate cancer cell survival/migration/invasion, cell cycle regulation, and apoptosis. miR-214 was differentially expressed between Caucasian and African American prostate cancer cells. Importantly, miR-214 overexpression in prostate cancer cells induced apoptosis, inhibiting cell proliferation and colony forming ability. miR-214 expression in prostate cancer cells also inhibited cell migration and 3D spheroid invasion. Mechanistically, miR-214 inhibited prostate cancer cell proliferation by targeting protein tyrosine kinase 6 (PTK6). Restoration of PTK6 expression attenuated the inhibitory effect of miR-214 on cell proliferation. Moreover, simultaneous inhibition of PTK6 by ibrutinib and miR-214 significantly reduced cell proliferation/survival. Our data indicates that miR-214 could act as a tumor suppressor in prostate cancer and could potentially be utilized as a biomarker and therapeutic target.

show abstract

“…PTK6 (Protein tyrosine kinase six) is a cytoplasmic non-receptor protein kinase thatis highly expressed in tumors such as breast cancer, bladder cancer, lung cancer, and ovarian carcinoma. It has been detected that PTK6 overexpression is correlate with the poor prognosis of bladder cancer ( 29 ), prostate cancer ( 30 ), and breast cancer ( 31 ). NRG3 (neuregulin three) is abundantly expressed in brain tissue.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Value of an Autophagy-Related Five-Gene Signature for Lower-Grade Glioma Patients

Guo

Wei

et al. 2021

Front. Oncol.

View full text Add to dashboard Cite

Background: Molecular characteristics can be good indicators of tumor prognosis and have been introduced into the classification of gliomas. The prognosis of patients with newly classified lower-grade gliomas (LGGs, including grade 2 and grade 3 gliomas) is highly heterogeneous, and new molecular markers are urgently needed.Methods: Autophagy related genes (ATGs) were obtained from Human Autophagy Database (HADb). From the Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA), gene expression profiles including ATG expression information and patient clinical data were downloaded. Cox regression analysis, receiver operating characteristic (ROC) analysis, Kaplan–Meier analysis, random survival forest algorithm (RSFVH) and stratification analysis were performed.Results: Through univariate Cox regression analysis, we found a total of 127 ATGs associated with the prognosis of LGG patients from TCGA dataset and a total of 131 survival-related ATGs from CGGA dataset. Using TCGA dataset as the training group (n = 524), we constructed a five-ATG signature (including BAG1, BID, MAP1LC3C, NRG3, PTK6), which could divide LGG patients into two risk groups with significantly different overall survival (Log Rank P < 0.001). Then we confirmed in the independent CGGA dataset that the five-ATG signature had the ability to predict prognosis (n = 431, Log Rank P < 0.001). We further discovered that the predictive ability of the five-ATG signature was better than the existing clinical indicators and IDH mutation status. In addition, the five-ATG signature could further classify patients after receiving radiotherapy or chemotherapy into groups with different prognosis.Conclusions: We identified a five-ATG signature that could be a reliable prognostic marker and might be therapeutic targets for autophagy therapy for LGG patients.

show abstract

Overexpression of PTK6 predicts poor prognosis in bladder cancer patients

Cited by 23 publications

References 24 publications

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

<p>SRF Potentiates Colon Cancer Metastasis and Progression in a microRNA-214/PTK6-Dependent Manner</p>

MicroRNA-214 targets PTK6 to inhibit tumorigenic potential and increase drug sensitivity of prostate cancer cells

Prognostic Value of an Autophagy-Related Five-Gene Signature for Lower-Grade Glioma Patients

Contact Info

Product

Resources

About