Graphene-Based Biosensors with High Sensitivity for Detection of Ovarian Cancer Cells

Ovarian cancer has the highest mortality rate in the world. Therefore, it is urgent but still challenging to develop an efficient circulating tumor cell (CTC) detection method to sensitively detect ovarian cancer. To address such issues, herein, for the first time, we present a novel CTC detection method for ovarian cancer cells by designing sensitive and rapid graphene-based biosensors. This graphene-based sensor, consisting of a cell pool and two electrodes, can be prepared by a conventional chip fabrication process. It demonstrates high-sensitivity detection even for several ovarian cancer cells by comparing the electrical signal before and after adding cell solution. Moreover, the graphene-based biosensors can perform rapid detection with good repeatability. This suggests that this novel method is possible to use for the early detection of ovarian cancer with very low CTC cell concentration. This work provides a novel and quick strategy to detect ovarian cancer and further judge or predict the risk of the transfer of ovarian cancer.

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Demonstration of a Flexible Graphene-Based Biosensor for Sensitive and Rapid Detection of Ovarian Cancer Cells

Nanoscale Research Letters ◽

10.1186/s11671-021-03633-9 ◽

2021 ◽

Vol 16 (1) ◽

Author(s):

Ling Han ◽

Qi Wan ◽

Ai Zheng ◽

Yunchuan Guo ◽

Yali Chen

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Rapid Detection ◽

Culture Medium ◽

Detection Method ◽

Low Cost ◽

Prediction Method ◽

High Sensitivity ◽

Circulating Tumor Cell ◽

Ovarian Cancer Cells

AbstractIt is significant to develop an efficient early detection and prediction method for ovarian cancer via a facile and low-cost approach. To address such issues, herein, we develop a novel circulating tumor cell (CTC) detection method to sensitively detect ovarian cancer by using a flexible graphene-based biosensor on polyethylene terephthalate (PET) substrate. The results show that the graphene-based flexible biosensor demonstrates sensitive and rapid detection for ovarian cancer cells: it delivers obvious different responses for cell culture medium and cancer solution, different cancer cells and cancer cell solution with different concentrations; it demonstrates high sensitivity for detecting several tens of ovarian cancer cells per ml; moreover, the flexible graphene biosensor is very suitable for rapid and sensitive detection of ovarian cancer cells within 5 s. This work provides a low-cost and facile graphene biosensor fabrication strategy to sensitively and rapidly detect / identify CTC ovarian cancer cells. Graphical Abstract

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Sorafenib controls the epithelial-mesenchymal transition of ovarian cancer cells via EGF and the CD44-HA signaling pathway in a cell type-dependent manner

Molecular Medicine Reports ◽

10.3892/mmr.2017.6773 ◽

2017 ◽

Vol 16 (2) ◽

pp. 1826-1836 ◽

Cited By ~ 7

Author(s):

Ga Bin Park ◽

Hyun-Suk Ko ◽

Daejin Kim

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Epithelial Mesenchymal Transition ◽

Ovarian Cancer Cells ◽

Dependent Manner ◽

Cell Type ◽

Mesenchymal Transition ◽

A Cell

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High sensitivity of ovarian cancer cells to the synthetic triterpenoid CDDO-Imidazolide

Cancer Letters ◽

10.1016/j.canlet.2009.03.018 ◽

2009 ◽

Vol 282 (2) ◽

pp. 214-228 ◽

Cited By ~ 20

Author(s):

Alessia Petronelli ◽

Ernestina Saulle ◽

Luca Pasquini ◽

Eleonora Petrucci ◽

Gualtiero Mariani ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

High Sensitivity ◽

Ovarian Cancer Cells

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PARP Inhibition Activates STAT3 in Both Tumor and Immune Cells Underlying Therapy Resistance and Immunosuppression In Ovarian Cancer

Frontiers in Oncology ◽

10.3389/fonc.2021.724104 ◽

2021 ◽

Vol 11 ◽

Author(s):

Antons Martincuks ◽

Jieun Song ◽

Adrian Kohut ◽

Chunyan Zhang ◽

Yi-Jia Li ◽

...

Keyword(s):

Ovarian Cancer ◽

Cancer Cells ◽

Tumor Cells ◽

Immune Cells ◽

Therapy Resistance ◽

Parp Inhibitors ◽

Parp Inhibition ◽

Ovarian Cancer Cells ◽

Before And After ◽

Immunosuppressive Cytokine

Despite the promising activity of poly(ADP-ribose) polymerase (PARP) inhibitors (PARPi) in many cancer types with defects in the DNA damage response the majority of the treated patients acquire PARPi resistance and succumb to their diseases. Consequently, there is an urgent need to identify the mechanisms of PARPi resistance. Here, we show that PARPi treatment promotes STAT3 activation in ovarian cancer cells, tumor-associated immune cells and fibroblasts, resulting in PARPi resistance and immunosuppression. Comparison of ovarian cancer patient-matched tumor biopsies before and after PARPi therapy revealed that STAT3 activity was significantly higher in tumor cells and tumor-associated immune cells and fibroblasts post PARPi treatment. Moreover, one-time PARPi treatment activated STAT3 both in tumor cells as well as diverse immune subsets and fibroblasts. PARPi-treated immune cells exhibited decreased expression of immunostimulatory interferon (IFN)-γ and Granzyme B while increasing immunosuppressive cytokine IL-10. Finally, we demonstrate that the acquisition of PARPi resistance in ovarian cancer cells was accompanied by increased STAT3 activity. Ablating STAT3 inhibited PARPi-resistant ovarian tumor cell growth and/or restored PARPi sensitivity. Therefore, our study has identified a critical mechanism intrinsic to PARPi that promotes resistance to PARPi and induces immunosuppression during PARPi treatment by activating STAT3 in tumor cells and tumor-associated immune cells/fibroblasts.

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Induction of VEGF secretion in ovarian cancer by PDGF BB

Journal of Clinical Oncology ◽

10.1200/jco.2007.25.18_suppl.5557 ◽

2007 ◽

Vol 25 (18_suppl) ◽

pp. 5557-5557

Author(s):

D. Matei ◽

S. Kelich ◽

L. Cao ◽

N. Menning ◽

R. Emerson ◽

...

Keyword(s):

Ovarian Cancer ◽

Tumor Growth ◽

Cancer Cells ◽

Serum Levels ◽

Ovarian Tumors ◽

Ovarian Cancer Cells ◽

P Value ◽

Serum Samples ◽

Before And After ◽

Tumor Growth And Metastasis

5557 Background: We identified the PDGFR as a potential target in epithelial ovarian carcinoma (EOC). This led us to test whether inhibition of the receptor affects ovarian cancer cell proliferation and survival and regulates other processes critical to tumor growth and metastasis. We postulated that the PDGF-PDGFR axis regulates VEGF secretion in EOC. Methods: VEGF secretion in ovarian tumors, cancer cells, serum and ascites was measured by IHC, Western Blot and ELISA. The HOG Gyn03–62 protocol was a phase II protocol for patients with recurrent platinum resistant EOC. Patients were treated with imatinib and docetaxel. Serum and tumor samples from patients enrolled on this protocol were analyzed for VEGF. Results: VEGF expression was quantified by IHC in ovarian tumors. Of 21 PDGFR expressing ovarian tumors, seven specimens immunostained strongly for VEGF and six tumors demonstrated 2+ VEGF reactive extracellular (secreted) material. PDGF and VEGF secretion was measured in 17 specimens of malignant EOC ascites. The levels of PDGF BB and VEGF were strongly correlated (Pearson coefficient =0.728, p-value=0.001), suggesting that the two pathways interconnect. There was no correlation between PDGF AA and VEGF levels. VEGF levels were measured in 13 paired serum samples from patients enrolled in the clinical protocol HOG: Gyn03–62, before and after treatment. VEGF serum levels were stabilized or decreased in 9 of 13 EOC patients treated with imatinib. In conditioned media from primary cells, VEGF secretion was four fold higher for tumor derived cells than for cells derived from the normal ovarian epithelium. PDGF increased ten-fold VEGF secretion in PDGFR expressing immortalized ovarian cells (C272/hTert/E7 and C889/hTert), while imatinib reduced VEGF production to basal state. The effects of imatinib were mediated via inhibition of Akt and MAPK pathways, by stabilization of HIF1 alpha. In ovarian cancer cells overexpressing consitutively active Akt, imatinib inhibited only partially the secretion of VEGF compared to control cells, suggesting that the PI3K/Akt pathway is significantly implicated in PDGF-stimulated VEGF secretion. Conclusions: These results suggest that by blocking the PDGFR, imatinib inhibits VEGF production. This affects the tumor microenvironment favoring ovarian tumor growth and metastasis. No significant financial relationships to disclose.

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