Bystander effects induced by electron beam-irradiated MCF-7 cells: a potential mechanism of therapy resistance

A new approach to fabricate TiNi surfaces combining the advantages of both monolithic and porous materials for implants is used in this work. New materials were obtained by depositing a porous TiNi powder onto monolithic TiNi plates followed by sintering at 1200 °C. Then, further modification of the material surface with a high-current-pulsed electron beam (HCPEB) was carried out. Three materials obtained (one after sintering and two after subsequent beam treatment by 30 pulses with different pulse energy) were studied by XRD, SEM, EDX, surface profilometry, and by means of electrochemical measurements, including OCP and EIS. Structural and compositional changes caused by HCPEB treatment were investigated. Surface properties of the samples during their storage in saline for 10 days were studied and a model experiment with cell growth (MCF-7) was carried out for the unmodified sample with an electron beam to detect cell appearance on different surface locations.

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Preparation and Electron-Beam Surface Modification of Novel TiNi Material for Medical Applications

10.20944/preprints202104.0141.v1 ◽

2021 ◽

Author(s):

Sergey G. Anikeev ◽

Anastasiia V. Shabalina ◽

Sergei A. Kulinich ◽

Nadezhda V. Artyukhova ◽

Darya R. Korsakova ◽

...

Keyword(s):

Electron Beam ◽

Model Experiment ◽

Material Surface ◽

High Current ◽

New Materials ◽

New Approach ◽

Pulsed Electron Beam ◽

Beam Surface ◽

Compositional Changes ◽

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A new approach to fabricate TiNi surfaces combining the advantages of both monolithic and porous materials for implants is used in this work. New materials were obtained by depositing a porous TiNi powder onto monolithic TiNi plates followed by sintering at 1200°C. Then, further modification of the material surface with a high-current-pulsed electron beam (HCPEB) was carried out. Three materials obtained (one after sintering and two after subsequent beam treatment by 20 and 30 pulses, respectively) were studied by XRD, SEM, EDX, EIS methods, profilometry and OCP measurements. Structural and compositional changes caused by HCPEB treatment were investigated. Surface properties of the samples during their storage in saline for 10 days were studied and a model experiment with cell growth (MCF-7) was carried out for the sample unmodified with electron beam to detect cell appearance on different surface locations.

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Key Role of Nuclear Factor-κB in the Cellular Pharmacokinetics of Adriamycin in MCF-7/Adr Cells: The Potential Mechanism for Synergy with 20(S)-Ginsenoside Rh2

Drug Metabolism and Disposition ◽

10.1124/dmd.112.045187 ◽

2012 ◽

Vol 40 (10) ◽

pp. 1900-1908 ◽

Cited By ~ 22

Author(s):

Jingwei Zhang ◽

Meng Lu ◽

Fang Zhou ◽

Haopeng Sun ◽

Gang Hao ◽

...

Keyword(s):

Nuclear Factor Κb ◽

Nuclear Factor ◽

Ginsenoside Rh2 ◽

Potential Mechanism ◽

Cellular Pharmacokinetics ◽

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Endocrine therapy resistance can be associated with high estrogen receptor α (ERα) expression and reduced ERα phosphorylation in breast cancer models

Endocrine Related Cancer ◽

10.1677/erc.1.01257 ◽

2006 ◽

Vol 13 (4) ◽

pp. 1121-1133 ◽

Cited By ~ 34

Author(s):

Barbara Kuske ◽

Catherine Naughton ◽

Kate Moore ◽

Kenneth G MacLeod ◽

William R Miller ◽

...

Keyword(s):

Breast Cancer ◽

Estrogen Receptor ◽

Cell Lines ◽

Therapy Resistance ◽

Estrogen Receptor Α ◽

Cancer Models ◽

Er Positive ◽

Tamoxifen Resistant ◽

Trefoil Factor 1 ◽

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Hormone-dependent estrogen receptor (ER)-positive breast cancer cells may adapt to low estrogen environments such as produced by aromatase inhibitors. In many instances, cells become insensitive to the effects of estrogen but may still retain dependence on ER. We have investigated the expression, function, and activation of ERα in two endocrine-resistant MCF-7 models to identify mechanisms that could contribute to resistance. While MCF-7/LCC1 cells are partially estrogen dependent, MCF-7/LCC9 cells are fully estrogen insensitive and fulvestrant and tamoxifen resistant. In both MCF-7/LCC1 and MCF-7/LCC9 cell lines, high expression of ERα was associated with enhanced binding to the trefoil factor 1 (TFF1) promoter in the absence of estrogen and increased transcription of TFF1 and progesterone receptor. In contrast to the observations derived from hypersensitive and supersensitive models, these cells were truly estrogen independent; nevertheless, removal of ERα by siRNA, or fulvestrant, a specific ER downregulator, inhibited growth indicating dependence on ERα. In the absence of estrogen, neither ERα Ser118 nor Ser167 were phosphorylated as frequently found in other ligand-independent cell line models. Addition of estrogen activated ERα Ser118 in MCF-7 and LCC1 cells but not in LCC9 cells. We suggest that the estrogen-independent growth within these cell lines is accounted for by high levels of ERα expression driving transcription and full estrogen independence explained by lack of ERα activation through Ser118.

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Role of Differentially Expressed Proteins in Acquired Resistance to Cdk4/6 Inhibitor in Breast Cancer

10.21203/rs.3.rs-556331/v1 ◽

2021 ◽

Author(s):

Binayak Kumar ◽

Peeyush Prasad ◽

Ragini Singh ◽

Ram Krishana Sahu ◽

Ashutosh Singh ◽

...

Keyword(s):

Breast Cancer ◽

Drug Targets ◽

Acquired Resistance ◽

Therapy Resistance ◽

Resistant Cell ◽

Molecular Signature ◽

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Resistant Cells

Abstract CDK4/6 inhibitors (Abemaciclib, Ab and Palbociclib, Pb) stop the G1-phase in cell-cycle being used to cure advanced stage of breast cancer (BC). Acquired resistance is a major challenge in BC therapy. The molecular signature of the therapy resistance for Ab and Pb drugs in BC should be explored. Here, we developed Ab/Pb-resistant cell-models and explored the molecular changes. Drug’s resistance cells were developed in MCF-7 cells by continuous drug treatment and it was confirmed by MTT-assay, PI-staining-microscopy, and real-time-qPCR. Global proteome profiling done by Labelled-free-Proteome-Orbitrap-Fusion-MS-MS technique. Bioinformatics tools used to analyse the proteome data. Ab-resistant and Pb-resistant MCF-7 cells showed increased tolerance for the respective drug. The BCL-2 and MCL-1 survival genes were up-regulated, while the apoptosis genes BAD, BAX, CASP-3 and PARP-1were down-regulated in the resistant cells. Expression of the MDR-1, ABCG2, ESR-1, CDK4, CDK6, and Cyclin-D1 genes were increased in both resistance cells. For proteomics, 237 and 239 proteins were expressed differently in the resistant Ab and Pb cells, respectively. The NUDT5, PEPD, ABAT, ATP1B1, GGCT, and SELENBP1 proteins were down-regulated and the SBSN, HSD17B10, CD9, PDIA3, PSMB4, SLC2A1, and VTN proteins were up-regulated in Ab-resistant cells. The NUDT5, PEPD, and GGCT proteins were down-regulated, while CD47, HIST1H2BN, LMNA, VTN, PSMB5, HBB, PSMA7, FLNB, PRDX4, VDAC1, GOT2, HSPA5, SERPINH1, EIF4A2, FTH, and VIM proteins were up-regulated in Pb-resistant cells. These proteins are a new set of prognostic markers and drug targets for overcoming the respective drug resistance. However, it is necessary to perform an in vivo or clinical assessment.

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Arsenic disulfide‑induced apoptosis and its potential mechanism in two‑ and three‑dimensionally cultured human breast cancer MCF‑7 cells

International Journal of Oncology ◽

10.3892/ijo.2018.4357 ◽

2018 ◽

Cited By ~ 1

Author(s):

Yuxue Zhao ◽

Kenji Onda ◽

Bo Yuan ◽

Sachiko Tanaka ◽

Anna Kiyomi ◽

...

Keyword(s):

Breast Cancer ◽

Human Breast Cancer ◽

Potential Mechanism ◽

Human Breast ◽

Induced Apoptosis ◽

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Potential mechanism of mycelium polysaccharide from Pholiota dinghuensis Bi in regulating the proliferation and apoptosis of human breast cancer MCF-7 cells through p38/MAPK pathway

Journal of Functional Foods ◽

10.1016/j.jff.2014.12.008 ◽

2015 ◽

Vol 12 ◽

pp. 375-388 ◽

Cited By ~ 11

Author(s):

Dan Gan ◽

Xiaoxiong Zeng ◽

Rui Hai Liu ◽

Hong Ye

Keyword(s):

Breast Cancer ◽

P38 Mapk ◽

Human Breast Cancer ◽

Mapk Pathway ◽

Potential Mechanism ◽

Human Breast ◽

P38 Mapk Pathway ◽

Proliferation And Apoptosis ◽

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TRIM47 activates NF-κB signaling via PKC-ε/PKD3 stabilization and contributes to endocrine therapy resistance in breast cancer

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2100784118 ◽

2021 ◽

Vol 118 (35) ◽

pp. e2100784118

Author(s):

Kotaro Azuma ◽

Kazuhiro Ikeda ◽

Takashi Suzuki ◽

Kenjiro Aogi ◽

Kuniko Horie-Inoue ◽

...

Keyword(s):

Breast Cancer ◽

Protein Kinase ◽

Cancer Patients ◽

Endocrine Therapy ◽

Cancer Biology ◽

Therapy Resistance ◽

Clinical Samples ◽

Breast Cancer Patients ◽

Endocrine Therapy Resistance ◽

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Increasing attention has been paid to roles of tripartite motif–containing (TRIM) family proteins in cancer biology, often functioning as E3 ubiquitin ligases. In the present study, we focus on a contribution of TRIM47 to breast cancer biology, particularly to endocrine therapy resistance, which is a major clinical problem in breast cancer treatment. We performed immunohistochemical analysis of TRIM47 protein expression in 116 clinical samples of breast cancer patients with postoperative endocrine therapy using tamoxifen. Our clinicopathological study showed that higher immunoreactivity scores of TRIM47 were significantly associated with higher relapse rate of breast cancer patients (P = 0.012). As functional analyses, we manipulated TRIM47 expression in estrogen receptor–positive breast cancer cells MCF-7 and its 4-hydroxytamoxifen (OHT)-resistant derivative OHTR, which was established in a long-term culture with OHT. TRIM47 promoted both MCF-7 and OHTR cell proliferation. MCF-7 cells acquired tamoxifen resistance by overexpressing exogenous TRIM47. We found that TRIM47 enhances nuclear factor kappa-B (NF-κB) signaling, which further up-regulates TRIM47. We showed that protein kinase C epsilon (PKC-ε) and protein kinase D3 (PKD3), known as NF-κB–activating protein kinases, are directly associated with TRIM47 and stabilized in the presence of TRIM47. As an underlying mechanism, we showed TRIM47-dependent lysine 27–linked polyubiquitination of PKC-ε. These results indicate that TRIM47 facilitates breast cancer proliferation and endocrine therapy resistance by forming a ternary complex with PKC-ε and PKD3. TRIM47 and its associated kinases can be a potential diagnostic and therapeutic target for breast cancer refractory to endocrine therapy.

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