Knockdown of KRT17 by siRNA induces antitumoral effects on gastric cancer cells

Chivu‐Economescu, Mihaela; Dragu, Denisa; Necula, Laura; Matei, Lilia; Enciu, Ana‐Maria; Bleoţu, Coralia; Diaconu, Carmen C.

doi:10.1007/s10120-017-0712-y

Cited by 57 publications

(42 citation statements)

References 29 publications

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“…33 The relationship between KRT17 and mTOR pathway has been reported in many studies. Chivu-Economescu et al 34 cancer mainly via mTOR pathway. Khanom et al 35 also reported KRT17 stimulated mTOR pathway which facilitating oral cancer growth.…”

Section: Discussionmentioning

confidence: 99%

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<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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Section: Discussionmentioning

confidence: 99%

“…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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“…[ 34 ] KRT17 has been shown to be a possible biomarker in GC promoting tumor growth, motility, and invasion. [ 35 ] Growing evidence suggest that BRIP1 may have an antioncogenic role, and downregulation of BRIP1 has been observed in multiple types of cancer. [ 36 ] On account of the unbalanced expression in specific gene pairs, which might play a more important role than individual genes, the remaining 11 genes might also play a role in CRC prognosis prediction.…”

Section: Discussionmentioning

confidence: 99%

Gene pair based prognostic signature for colorectal colon cancer

Shu

Tong

et al. 2018

Medicine

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“…Most studies report that the use of miRNA and siRNA reduces the tumorigenicity of various types of solid cancers [ 113 , 114 , 115 , 116 , 117 , 118 , 119 ]. These molecules mediate RNA interference, inhibiting the translation of mRNA targets.…”

Section: Engineering Ev-based Cancer Therapymentioning

confidence: 99%

Extracellular Vesicle-Based Nucleic Acid Delivery: Current Advances and Future Perspectives in Cancer Therapeutic Strategies

et al. 2020

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Extracellular vesicles (EVs) are sophisticated and sensitive messengers released by cells to communicate with and influence distant and neighboring cells via selective transfer of bioactive content, including protein lipids and nucleic acids. EVs have therefore attracted broad interest as new and refined potential therapeutic systems in many diseases, including cancer, due to their low immunogenicity, non-toxicity, and elevated bioavailability. They might serve as safe and effective vehicles for the transport of therapeutic molecules to specific tissues and cells. In this review, we focus on EVs as a vehicle for gene therapy in cancer. We describe recent developments in EV engineering to achieve efficient intracellular delivery of cancer therapeutics and avoid off-target effects, to provide an overview of the potential applications of EV-mediated gene therapy and the most promising biomedical advances.

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Knockdown of KRT17 by siRNA induces antitumoral effects on gastric cancer cells

Abstract: Our results highlight KRT17 as a possible biomarker in gastric cancer promoting tumor growth, motility, and invasion, and suggest that KRT17 can be a valuable molecular target for development of anti-gastric cancer-specific therapies.

Cited by 57 publications

References 29 publications

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

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

Gene pair based prognostic signature for colorectal colon cancer

Extracellular Vesicle-Based Nucleic Acid Delivery: Current Advances and Future Perspectives in Cancer Therapeutic Strategies

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