Dysregulation of YAP by ARF Stimulated with Tea-derived Carbon Nanodots

Xie, Yingqiu; Sun, Qinglei; Nurkesh, Ayan; Jiang, Lu; Kauanova, Sholpan; Feng, Jinhong; Tursynkhan, Darkhan; Kassymbek, Aishabibi; Karibayev, Mirat; Duisenova, Korlan; Fan, Haiyan; Wang, Xiao; Manarbek, Limara; Maipas, Aisulu; Chen, Zhenbang; Balanay, Mannix P.

doi:10.1038/s41598-017-16441-y

Cited by 19 publications

(20 citation statements)

References 43 publications

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“…For instance, C‐dots synthesized from ginger inhibit HepG2 cells growth in vivo of mouse model . C‐dots derived from green tea inhibit the growth of MCF‐7, MDAMB‐231 breast cancers, and prostate cancer cells as we and others showed . C‐dots derived from date pits ( Phoenix dactylifera ) inhibit cancerous cell migration with changes in cytoskeleton .…”

Section: Introductionmentioning

confidence: 58%

“…C‐dots derived from date pits ( Phoenix dactylifera ) inhibit cancerous cell migration with changes in cytoskeleton . Mechanistically, tea derived C‐dots were found to inhibit cancer cell growth and interact with nuclear protein ARF and regulate hippo pathway . As regular therapies may easily induce drug resistance, there is a huge demand for an alternative approach.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, people attempted to use nanoparticles in drug delivery . Given that C‐dots with their small average size, and small enough to be able to enter into nucleus, they may potentially interact with DNA leading to the DNA damage induced cell death. On the other hand, they may cause the mediated signaling cascade.…”

Section: Introductionmentioning

confidence: 99%

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Date Pit Carbon Dots Induce Acidic Inhibition of Peroxidase and Disrupt DNA Repair in Antibacteria Resistance

et al. 2019

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Carbon nanodots (C‐dots) are emerging as a new type of promising agent in anticancer, imaging, and new energy. Reports as well as the previous research indicate that certain C‐dots can enhance targeted cancer therapy. However, in‐depth mechanisms for such anticancer effect remain unclear. In this work, treatment provided by the date pit‐derived C‐dots, exhibits significant DNA damage; Annexin V/7‐AAD‐mediated apoptosis, and G2/M cell cycle arrest in prostate cancer cells. The application of C‐dots to the cell generally leads to acidulation of the cell medium, cooperated with membrane compact. The date pit‐derived C‐dots are observed inhibiting the horseradish peroxidase. Moreover, the C‐dots disrupt likely through nucleotide excision DNA repair at low dose during DNA ligation step suggesting the antimicrobial effect and targeting Pim‐1, EGFR, mTOR, and DNA damage pathways in cancer cells. For the first time the detailed and novel mechanisms underlying the C‐dots, derived from the date‐pit, as an efficient, low‐cost, and green nanomaterial are reveled for cancer therapy and anti‐infection.

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Section: Introductionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

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Date Pit Carbon Dots Induce Acidic Inhibition of Peroxidase and Disrupt DNA Repair in Antibacteria Resistance

et al. 2019

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“…Based on our recent findings on MMP family protein evolution and translocation, more studies are needed to elucidate both NLMP and disease evolutions [62]. Recently we found YAP is also a shuttling protein localized in cytosol, nucleus and membrane and is regulated by nuclear protein ARF [63]. In addition, MMP nuclear localization correlates to ARF elevation in prostate cancer cells [64].…”

Section: Discussionmentioning

confidence: 99%

Systematic analysis of NLMP suggests nuclear localization of RTK/MET kinases resemble cancer cell clearance

Xie

Nurkesh

Ibragimova

et al. 2019

J Exp Clin Cancer Res

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BackgroundSome membrane proteins can translocate into the nucleus, defined as nuclear localized membrane proteins (NLMPs), including receptor tyrosine kinases (RTKs). We previously showed that nuclear MET (nMET), a member of RTKs, mediates cancer stem-like cells self-renewal to promote cancer recurrence. However, it is unknown that nMET or mMET, which is the ancestor in the evolution of cancer cell survival and clearance. Here, we aim to study the NLMP functions in cell death, differentiation and survival.MethodWe applied the systematic reanalysis of functional NLMP and clinical investigations of nMET from databases. In addition, we used soft agar assay, immunoblotting, flow cytometry, and immunofluorescence confocal microscopy for examinations of nMET functions including stem-like cell formation, cell signaling, cell cycle regulation, and co-localization with regulators of cell signaling. ShRNA, antibody of recognizing surface membrane MET based treatment were used to downregulate endogenous nMET to uncover its function.ResultsWe predicted and demonstrated that nMET and nEGFR are most likely not ancestors. nMET overexpression induces both cell death and survival with drug resistance and stem cell-like characters. Moreover, the paradoxical function of nMET in both cell death and cell survival is explained by the fact that nMET induces stem cell-like cell growth, DNA damage repair, to evade the drug sensitization for survival of single cells while non-stem cell-like nMET expressing single cells may undergo clearance by cell death through cell cycle arrest induced by p21.ConclusionTaken together, our data suggest a link between nuclear RTK and cancer cell evolutionary clearance via cell death, and drug resistance for survival through stemness selection. Targeting evolved nuclear RTKs in cancer stem cells would be a novel avenue for precision cancer therapy.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-1004-z) contains supplementary material, which is available to authorized users.

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“…As an example, carbon dots prepared from a spice have been found to be able to inhibit tumor growth in a xenograft model (17). Another study found that carbon dots prepared from tea can bind to certain amino acids on ARF and colocalize with ARF in the nucleus, thus sensitizing cancer cells to rapamycin (18,19). The current study used an atomic carbon material (Australian patent number: 2005230336, Figure 1).…”

Section: Introductionmentioning

confidence: 99%