Molecular characterization of breast cancer cell lines through multiple omic approaches

Smith, Shari E.; Mellor, Paul; Ward, Alison K; Kendall, Stephanie; McDonald, Megan; Vizeacoumar, Frederick S.; Napper, Scott; Anderson, Deborah H.

doi:10.1186/s13058-017-0855-0

Cited by 66 publications

(57 citation statements)

References 61 publications

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“…To identify essential RBPs per BC molecular subtype, we first updated subtypes by merging data from Smith et al 40 , Dai et al 41 , and Kao et al 42 (Supp. Table 10).…”

Section: Resultsmentioning

confidence: 99%

“…RBPs cancer dependency scores from CERES 11 (1288 available RBPs) and DEMETER2 12,13 (1290 available RBPs) were obtained from the Dependency Map (DepMap) portal (https://depmap.org/portal/). Molecular subtypes of 82 (DEMETER2 12,13 ) and 28 (CERES 11 ) BC cell lines were obtained from Smith et al 40 , Dai et al 41 , and Kao et al 42 (Supp. Table 10)…”

Section: Methodsmentioning

confidence: 99%

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In silico analyses reveal new putative Breast Cancer RNA-binding proteins

Guerrero

López‐Cortés

García-Cárdenas

et al. 2020

Preprint

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Breast cancer (BC) is the leading cause of cancer-associated death among women worldwide. Despite treatment efforts, advanced BC with distant organ metastases is considered incurable. A better understanding of BC molecular processes is therefore of great interest to identify new therapeutic targets. Although large-scale efforts, such as The Cancer Genome Atlas (TCGA), have completely redefined cancer drug development, diagnosis, and treatment, additional key aspects of tumor biology remain to be discovered. In that respect, post-transcriptional regulation of tumorigenesis represents an understudied aspect of cancer research. As key regulators of this process, RNA-binding proteins (RBPs) are emerging as critical modulators of tumorigenesis but only few have defined roles in BC. To unravel new putative BC RBPs, we have performed in silico analyses of all human RBPs in three major cancer databases (TCGA-Breast Invasive Carcinoma, the Human Protein Atlas, and the Cancer Dependency Map project) along with complementary bioinformatics resources (STRING protein-protein interactions and the Network of Cancer Genes 6.0). Thus, we have identified six putative BC progressors (MRPL13, SCAMP3, CDC5L, DARS2, PUF60, and PLEC), and five BC suppressors RBPs (SUPT6H, MEX3C, UPF1, CNOT1, and TNKS1BP1). These proteins have never been studied in BC but show similar cancer-associated features than well-known BC proteins. Further research should focus on the mechanisms by which these proteins promote or suppress breast tumorigenesis, holding the promise of new therapeutic pathways along with novel drug development strategies.

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“…To identify essential RBPs per BC molecular subtype, we first updated subtypes by merging data from Smith et al 40 , Dai et al 41 , and Kao et al 42 (Supp. Table 10).…”

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

In silico analyses reveal new putative Breast Cancer RNA-binding proteins

Guerrero

López‐Cortés

García-Cárdenas

et al. 2020

Preprint

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“…However, no studies have described a comprehensive connection between activation of these signaling pathways and proliferation of breast cancer cells. The difficulty to assess this connection is compounded by the fact that the vast majority of available breast cancer cell lines contain mutations involved in the PI3K/Akt/mTOR pathway (38). Although most ER+ breast cancer cell lines contain mutations within this pathway, the specific mutations have distinctly different effects on the activation of the PI3K/Akt/mTOR pathway.…”

Section: Discussionmentioning

confidence: 99%

GREB1 regulates proliferation of estrogen receptor positive breast cancer through modulation of PI3K/Akt/mTOR signaling

Haines

Klingensmith

Burd

2019

Preprint

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19Over 70% of breast cancers express the estrogen receptor (ER) and depend on ER 20 activity for survival and proliferation. While hormone therapies that target receptor activity are 21 initially effective, patients invariably develop resistance which is often associated with activation 22 of the PI3K/Akt/mTOR pathway. While the mechanism by which estrogen regulates proliferation 23is not fully understood, one gene target of ER, growth regulation by estrogen in breast cancer 1 24 (GREB1), is required for hormone-dependent proliferation. However, the molecular function by 25 which GREB1 regulates proliferation is unknown. Herein, we validate that knockdown of GREB1 26 results in growth arrest and that exogenous GREB1 expression initiates oncogene-induced 27 senescence, suggesting that an optimal level of GREB1 expression is necessary for 28 proliferation of breast cancer cells. Under both of these conditions, GREB1 is able to regulate 29 signaling through the PI3K/Akt/mTOR pathway. GREB1 acts intrinsically through PI3K to 30 regulate PIP 3 levels and Akt activity. Critically, growth suppression of estrogen-dependent 31 breast cancer cells by GREB1 knockdown is rescued by expression of constitutively activated 32Akt. Together, these data identify a novel molecular function by which GREB1 regulates breast 33 cancer proliferation through Akt activation and provides a mechanistic link between estrogen 34 signaling and the PI3K pathway. 35 36

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“…As a prerequisite for studying SETD3 function in vitro, we characterized its expression by quantitative 26 . Only MCF-7 cells showed a p53 WT status.…”

Section: Expression Of Setd3 In Cell Lines Representing Different Molmentioning

confidence: 99%

SETD3 acts as a prognostic marker in breast cancer patients and modulates the viability and invasion of breast cancer cells

Hassan

Rutsch

Győrffy

et al. 2020

Sci Rep

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In several carcinomas, the SET Domain Containing 3, Actin Histidine Methyltransferase (SETD3)is associated with oncogenesis. However, there is little knowledge about the role of SETD3 in the progression and prognosis of breast cancer. In this study, we first analyzed the prognostic value of SETD3 in breast cancer patients using the database of the public Kaplan-Meier plotter. Moreover, in vitro assays were performed to assess the role of SETD3 in the viability and capacity of invasion of human breast cancer cell lines. We observed that the high expression of SETD3 was associated with better relapse-free survival (RFS) of the whole collective of 3,951 patients, of Estrogen Receptorpositive, and of Luminal A-type breast cancer patients. However, in patients lacking expression of estrogen-, progesterone-and HER2-receptor, and those affected by a p53-mutation, SETD3 was associated with poor RFS. In vitro analysis showed that SETD3 siRNA depletion affects the viability of triple-negative cells as well as the cytoskeletal function and capacity of invasion of highly invasive MDA-MB-231 cells. Interestingly, SETD3 regulates the expression of other genes associated with cancer such as β-actin, FOXM1, FBXW7, Fascin, eNOS, and MMP-2. Our study suggests that SETD3 expression can act as a subtype-specific biomarker for breast cancer progression and prognosis.MTT proliferation assay. SETD3 depleted cells or controls (5 × 10 3 ) were plated in 96-well plates with DMEM medium (without phenol red) (Gibco ® , cat. No. 31053028, Germany) with FCS and incubated for 96 hours. After the incubation time, the medium was removed completely and cells were incubated with 20 µl/well of 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) (cat. No. M2128-1G), at 5 mg/ml for 4 hours, at 37 °C. Subsequently, 100 µl of Stopping buffer, pH 4.7 composed of 10% (w/v) sodium dodecyl sulfate (SDS) (cat. No. 3599286) and 50% (v/v) N,) was added to stop the reaction and dissolve the formazan crystals. The absorbance was measured in a VersaMax ® Microplate Reader (Molecular Devices, Sunnyvale, CA, USA) at a wavelength of 595 nm. The proliferation of the control cells was defined as 100%. Results were derived from three independent sets of triplicate experiments. MTT, SDS, and N,N-Dimethyl formamide were from Sigma-

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Molecular characterization of breast cancer cell lines through multiple omic approaches

Cited by 66 publications

References 61 publications

In silico analyses reveal new putative Breast Cancer RNA-binding proteins

In silico analyses reveal new putative Breast Cancer RNA-binding proteins

GREB1 regulates proliferation of estrogen receptor positive breast cancer through modulation of PI3K/Akt/mTOR signaling

SETD3 acts as a prognostic marker in breast cancer patients and modulates the viability and invasion of breast cancer cells

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