KRT17 confers paclitaxel-induced resistance and migration to cervical cancer cells

Li, Jinyuan; Chen, Qiufang; Deng, Zhendong; Rothenberg, Marc E.; Liu, Hong; Ying, Tao; Wang, Xiaoyu; Lin, Shaoqiang; Liu, Naihua

doi:10.1016/j.lfs.2019.03.065

Cited by 35 publications

(28 citation statements)

References 37 publications

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“…It is well established that cancer cells would acquire some features similar to cancer stem cells, which confers the capacity to drug efflux or other mechanisms to resist chemotherapy cytotoxicity [31]. Data from studies of cervical cancer has proven that KRT17 depletion leads to drug sensitivity [20,27]. In our study, the interference of KRT17 indeed increased cisplatin sensitivity, and this sensitivity to cisplatin may result from the EMT process reversal.…”

Section: Discussionsupporting

confidence: 57%

“…Chiang and colleagues demonstrates the potential role of KRT17 in EMT process in areca nut-induced cancer [30]. Recent studies conducted on cervical cancer cells [20] and non-small cell lung cancer cells [31] also confirm the contribution of KRT17 in the EMT process. We noticed that KRT17 knockdown impaired EMT in BCa cell lines, in accordance with these previous reports.…”

Section: Discussionmentioning

confidence: 94%

“…Previous studies have linked KRT17 expression with paclitaxel resistance in cervical cancer [20]. To determine whether depletion of KRT17 could influence the cisplatin tolerance, BCa cell lines T24 and 5637, transfected with shKRT17 were incubated with indicated concentration of cisplatin for 24 h and 48 h. As shown in Figure 4A and 4B, survival T24 cells with KRT17 interference was dramatically reduced compared to the counterpart transfected with negative control, after incubation for 24 h and 48 h. A similar result was also investigated in 5637 cells (Fig.…”

Section: Knockdown Of Krt17 Enhanced the Sensitivity To Cisplatin Of mentioning

confidence: 99%

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Keratin 17 knockdown suppressed malignancy and cisplatin tolerance of bladder cancer cells, as well as the activation of AKT and ERK pathway

Ruan

et al. 2021

Folia Histochem Cytobiol.

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 94%

Section: Knockdown Of Krt17 Enhanced the Sensitivity To Cisplatin Of mentioning

confidence: 99%

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Keratin 17 knockdown suppressed malignancy and cisplatin tolerance of bladder cancer cells, as well as the activation of AKT and ERK pathway

Ruan

et al. 2021

Folia Histochem Cytobiol.

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“…Depianto et al 14 first reported that KRT17 promoted epithelial proliferation and tumor growth in skin. Previous studies illustrated that KRT17 is overexpressed in many cancers, including cervical cancer, 15 gastric cancer, 16 and lung cancer. 17 However, the relationship between KRT17 and pancreatic cancer is not exactly clear.…”

Section: Introductionmentioning

confidence: 99%

<p>KRT17 Functions as a Tumor Promoter and Regulates Proliferation, Migration and Invasion in Pancreatic Cancer via mTOR/S6k1 Pathway</p>

Li¹,

Ni²,

Tang³

et al. 2020

CMAR

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Background: Pancreatic cancer (PC) is one of the most well-known malignancies with high mortality, but the underlying mechanism of PC remains unknown. Keratin17 (KRT17) expression has been reported in many malignancies, but its functions in PC are not clear. The aim of our study was to evaluate KRT17 expression and its potential role in PC. Methods: The online databases GEPIA and THPA were used to identify KRT17 expression in tissues. Quantitative real-time PCR (qRT-PCR) was used to determine KRT17 expression in cell lines. Ki67 and ROS levels were detected by immunofluorescence assay and a 2ʹ,7ʹdichlorodihydrofluorescein diacetate (DCFH-DA) probe. KRT17 downregulation was induced by the small interfering RNA (siRNA) technique. Proliferation function was evaluated by colony formation assay and RTCA. Migration and invasion were evaluated by transwell migration assay. A Western blot assay was used to detect protein levels. Results: KRT17 was overexpressed in PC tissues compared to that in normal tissues. The results showed that Ki67 and ROS levels were decreased in pancreatic cancer cells after transfection with siKRT17. After KRT17 downregulation in PC cell lines, cell viability functions, including proliferation, migration and invasion, and mTOR/S6K1 phosphorylation levels were attenuated. Conclusion: KRT17 knockdown significantly inhibited proliferation, migration and invasion in pancreatic cancer cells.

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“…Keratins are also important in the context of oncogenesis, with elevated expression of KRT17 that was associated with poor prognosis having been observed in the context of colorectal cancer, pancreatic cancer, and non-small cell lung cancer [7,8]. Prior evidence suggests that KRT17 can in uence tumor proliferation and metastasis [9][10][11][12][13], but its function in HCC remains to be de ned.…”

Section: Introductionmentioning

confidence: 99%

KRT17 Serves as an Oncogene and a Predictor of Poor Survival in Hepatocellular Carcinoma Patients

chen¹,

Chen²,

Tian³

et al. 2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is the second most common cancer-associated cause of death globally. It is thus vital that novel diagnostic and prognostic biomarkers associated with early-stage HCC be identified. While keratin 17 (KRT17) has previously been reported to be associated with certain cancer types, its relationship with HCC remains to be defined. Methods：The expression of KRT17 in the TCGA LIHC database and in 44 pairs of HCC patient samples was assessed via qRT-PCR, western blotting, and immunohistochemical staining. The prognostic relevance of KRT17 was assessed using Kaplan-Meir curves, while important cancer- and KRT17-related biological processes were defined through gene set enrichment analysis (GSEA). The functional link between KRT17 expression and tumor cell proliferation/survival was assessed through flow cytometry, colony formation assay, CCK-8 assay, and subcutaneous tumor model approaches. Protein-protein interaction (PPI) networks and analyses of immune cell infiltration were also employed to define key signaling pathways associated with KRT17 expression in HCC. Results：HCC tissue samples exhibited increased KRT17 mRNA and protein expression that was predictive of poorer patient survival (P<0.001). GSEA and functional experiments revealed that KRT17 functioned as a regulator of HCC tumor cell survival, proliferation, and cell cycle progression in vitro and in vivo. PPI network analyses also revealed that KRT17 expression was linked to immune cell infiltration and activation in patients with HCC. Conclusion: We found that increased KRT17 levels were associated with poorer survival, more aggressive disease, and altered immune cell infiltration in patients suffering from HCC. As such, KRT17 may function as an oncogene and a prognostic biomarker in this cancer type.

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KRT17 confers paclitaxel-induced resistance and migration to cervical cancer cells

Cited by 35 publications

References 37 publications

Keratin 17 knockdown suppressed malignancy and cisplatin tolerance of bladder cancer cells, as well as the activation of AKT and ERK pathway

Keratin 17 knockdown suppressed malignancy and cisplatin tolerance of bladder cancer cells, as well as the activation of AKT and ERK pathway

<p>KRT17 Functions as a Tumor Promoter and Regulates Proliferation, Migration and Invasion in Pancreatic Cancer via mTOR/S6k1 Pathway</p>

KRT17 Serves as an Oncogene and a Predictor of Poor Survival in Hepatocellular Carcinoma Patients

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