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Higher Glucose Enhances Breast Cancer Cell Aggressiveness: Nutrition and Cancer: Vol 0, No 0
Cancer cells overexpress several transcription factors and motor proteins, such as NFkB and kinesin, to accommodate their high energy demand as well as migratory needs via enhanced glycolysis. We hypothesize that high glucose drives cancer progression and cell aggressiveness by decreasing actin expression, increasing NFkB, and kinesin expressions, and by activating Epithelial Mesenchymal Transition (EMT). Using lowly metastatic MCF-7 and highly metastatic MDA-MB231 (MB231) breast cancer cells – highly incident cancer types – we establish how glucose metabolism regulates actin and the biochemical changes that lead to alterations of cell mechanical properties. We find that higher glucose (15 and 30 mM) increases glycolytic enzymes, glucose uptake, migration speed, kinesin, Ki-67, and NFkB expressions (biomarkers), and hybrid EMT phenotype activation (adhesion molecules/cadherins). Downregulation of actin, increased expressions of motor protein and NFkB, and decreased nuclear stiffness – induced by higher glucose – result in a significant increase in the migration speed. Moreover, glucose deprivation using the glucose analog 2-deoxyglucose decreases significantly the migration speed in both cancer cells. Thus, higher glucose promotes a more aggressive phenotype that promises to be a new target for cancer therapy and can help prevent cancer progression in diabetic patients by inhibiting glucose activated mechanisms.
glucose  invasion  231_cells  MCF-7 
18 days ago by Segalllab
The tumor cell‐secreted matricellular protein WISP1 drives pro‐metastatic collagen linearization | The EMBO Journal
I wonder how much of this is increasing the pore size to make it easier for cells to move, since there was not a big gene expression effect?

Collagen linearization is a hallmark of aggressive tumors and a key pathogenic event that promotes cancer cell invasion and metastasis. Cell‐generated mechanical tension has been proposed to contribute to collagen linearization in tumors, but it is unknown whether other mechanisms play prominent roles in this process. Here, we show that the secretome of cancer cells is by itself able to induce collagen linearization independently of cell‐generated mechanical forces. Among the tumor cell‐secreted factors, we find a key role in this process for the matricellular protein WISP1 (CCN4). Specifically, WISP1 directly binds to type I collagen to promote its linearization in vitro (in the absence of cells) and in vivo in tumors. Consequently, WISP1‐induced type I collagen linearization facilitates tumor cell invasion and promotes spontaneous breast cancer metastasis, without significantly affecting gene expression. Furthermore, higher WISP1 expression in tumors from cancer patients correlates with faster progression to metastatic disease and poor prognosis. Altogether, these findings reveal a conceptually novel mechanism whereby pro‐metastatic collagen linearization critically depends on a cancer cell‐secreted factor.


Extracellular matrix collagen linearization is associated with aggressive tumors and promotes metastasis. The tumor cell‐secreted factor WISP1 induces collagen linearization independently of cell‐generated mechanical forces.

Breast carcinoma cells secrete WISP1 to induce collagen linearization.
WISP1 specifically remodels type I collagen.
TGF‐β1 promotes collagen linearization by inducing WISP1 expression.
WISP1‐induced collagen linearization facilitates tumor cell invasion and promotes spontaneous breast cancer metastasis.
Higher expression of WISP1 in tumors from cancer patients correlates with faster progression to metastatic disease.
collagen_fibers  231_cells  invasion  fibrillogenesis 
28 days ago by Segalllab
A Human Organotypic Microfluidic Tumor Model Permits Investigation of the Interplay between Patient-Derived Fibroblasts and Breast Cancer Cells | Cancer Research
Tumor–stroma interactions significantly influence cancer cell metastasis and disease progression. These interactions are partly comprised of the cross-talk between tumor and stromal fibroblasts, but the key molecular mechanisms within the cross-talk that govern cancer invasion are still unclear. Here, we adapted our previously developed microfluidic device as a 3D in vitro organotypic model to mechanistically study tumor–stroma interactions by mimicking the spatial organization of the tumor microenvironment on a chip. We cocultured breast cancer and patient-derived fibroblast cells in 3D tumor and stroma regions, respectively, and combined functional assessments, including cancer cell migration, with transcriptome profiling to unveil the molecular influence of tumor–stroma cross-talk on invasion. This led to the observation that cancer-associated fibroblasts (CAF) enhanced invasion in 3D by inducing expression of a novel gene of interest, glycoprotein nonmetastatic B (GPNMB), in breast cancer cells, resulting in increased migration speed. Importantly, knockdown of GPNMB blunted the influence of CAF on enhanced cancer invasion. Overall, these results demonstrate the ability of our model to recapitulate patient-specific tumor microenvironments to investigate the cellular and molecular consequences of tumor–stroma interactions.

Significance: An organotypic model of tumor–stroma interactions on a microfluidic chip reveals that CAFs promote invasion by enhancing expression of GPNMB in breast cancer cells.
cafs  invasion  microfluidics  SUM159  MCF7  231_cells 
7 weeks ago by Segalllab
The actin cytoskeletal architecture of estrogen receptor positive breast cancer cells suppresses invasion | Nature Communications
Interesting point that estrogen stimulates evl to generate cables that suppress invasion.

Estrogen promotes growth of estrogen receptor-positive (ER+) breast tumors. However, epidemiological studies examining the prognostic characteristics of breast cancer in postmenopausal women receiving hormone replacement therapy reveal a significant decrease in tumor dissemination, suggesting that estrogen has potential protective effects against cancer cell invasion. Here, we show that estrogen suppresses invasion of ER+ breast cancer cells by increasing transcription of the Ena/VASP protein, EVL, which promotes the generation of suppressive cortical actin bundles that inhibit motility dynamics, and is crucial for the ER-mediated suppression of invasion in vitro and in vivo. Interestingly, despite its benefits in suppressing tumor growth, anti-estrogenic endocrine therapy decreases EVL expression and increases local invasion in patients. Our results highlight the dichotomous effects of estrogen on tumor progression and suggest that, in contrast to its established role in promoting growth of ER+ tumors, estrogen has a significant role in suppressing invasion through actin cytoskeletal remodeling.
estrogen_receptor  MCF7  invasion  evl 
9 weeks ago by Segalllab
Cadherin-11 localizes to focal adhesions and promotes cell–substrate adhesion | Nature Communications
Cadherin receptors have a well-established role in cell–cell adhesion, cell polarization and differentiation. However, some cadherins also promote cell and tissue movement during embryonic development and tumour progression. In particular, cadherin-11 is upregulated during tumour and inflammatory cell invasion, but the mechanisms underlying cadherin-11 stimulated cell migration are still incompletely understood. Here, we show that cadherin-11 localizes to focal adhesions and promotes adhesion to fibronectin in Xenopus neural crest, a highly migratory embryonic cell population. Transfected cadherin-11 also localizes to focal adhesions in different mammalian cell lines, while endogenous cadherin-11 shows focal adhesion localization in primary human fibroblasts. In focal adhesions, cadherin-11 co-localizes with β1-integrin and paxillin and physically interacts with the fibronectin-binding proteoglycan syndecan-4. Adhesion to fibronectin mediated by cadherin-11/syndecan-4 complexes requires both the extracellular domain of syndecan-4, and the transmembrane and cytoplasmic domains of cadherin-11. These results reveal an unexpected role of a classical cadherin in cell–matrix adhesion during cell migration.
cdh11  focal_adhesions  fibroblasts  invasion 
june 2019 by Segalllab
Home :: Ivy Glioblastoma Atlas Project
The Ivy Glioblastoma Atlas Project includes the following data sets

ISH: Image data at cellular resolution of in situ hybridization (ISH) tissue sections and adjacent hematoxylin and eosin (H&E)-stained sections annotated for anatomic structures
Anatomic Structures ISH Survey: Primary screen of 8 tumors with probes for 343 genes enriched in glioblastoma.
Anatomic Structures ISH for Enriched Genes: Subsequent screen of 29 tumors with probes for 37 genes enriched in glioblastoma structures identified in Anatomic Structures RNA-Seq Study (see below).
Cancer Stem Cells ISH Survey: Primary screen of 16 tumors with probes for 55 genes enriched in putative cancer stem cells, resulting in a 20 probe reference set, which was then used in an extensive screen of 42 tumors.
Cancer Stem Cells ISH for Enriched Genes: Subsequent screen of 37 tumors with probes for 76 genes enriched in clusters of putative cancer stem cells identified in the Cancer Stem Cells RNA-Seq Study (see below).

RNA-Seq: RNA sequencing data for anatomic structures identified in the Anatomic Structures ISH Survey and putative cancer stem cell clusters isolated by laser microdissection
Anatomic Structures RNA-Seq: Screen of 5 structures (Leading Edge, Infiltrating Tumor, Cellular Tumor, Microvascular Proliferation, and Pseudopalisading Cells Around Necrosis) identified by H&E staining. A total of 122 RNA samples were generated from 10 tumors.
Cancer Stem Cells RNA-Seq: Screen of 35 clusters of putative cancer stem cells identified by ISH with a 17 reference probe subset (validated in the Cancer Stem Cells ISH Survey). A total of 148 RNA samples were generated from 34 tumors.

Specimen Metadata: De-identified clinical data for each patient and tumor.

Related Resources
Ivy GAP Clinical and Genomic Database: Partner database with additional clinical, genomic, and transcriptome data for each donor and tumor. Registration required for access to this database.
The Cancer Genome Atlas (TCGA): NIH-funded initiative for genomic mapping of cancers, including glioblastoma.
gbm  rnaseq  invasion 
june 2019 by Segalllab
Oncotarget | Elevated Orai1 expression mediates tumor-promoting intracellular Ca2+ oscillations in human esophageal squamous cell carcinoma
see 40 to 60 sec oscillations in ca that are reduce with ORAI1 KD
Effective treatment as well as prognostic biomarker for malignant esophageal squamous cell carcinoma (ESCC) is urgently needed. The present study was aimed at identifying oncogenic genes involving dysregulated intracellular Ca2+ signaling, which is known to function importantly in cellular proliferation and migration. Tumors from patients with ESCC were found to display elevated expression of Orai1, a store-operated Ca2+ entry (SOCE) channel, and the high expression of Orai1 was associated with poor overall and recurrence-free survival. In contrast to the quiescent nature of non-tumorigenic epithelial cells, human ESCC cells exhibited strikingly hyperactive in intracellular Ca2+ oscillations, which were sensitive to treatments with Orai1 channel blockers and to orai1 silencing. Moreover, pharmacologic inhibition of Orai1 activity or reduction of Orai1 expression suppressed proliferation and migration of ESCC in vitro and slowed tumor formation and growth in in vivo xenografted mice. Combined, these findings provide the first evidence to imply Orai1 as a novel biomarker for ESCC prognostic stratification and also highlight Orai1-mediated Ca2+ signaling pathway as a potential target for treatment of this deadly disease.
ORAI1  calcium  oscillations  invasion 
may 2019 by Segalllab
ORAI channels and cancer - ScienceDirect
useful overview
Cancer is a major cause of death. The diversity of cancer types and the propensity of cancers to acquire resistance to therapies, including new molecularly targeted and immune-based therapies, drives the search for new ways to understand cancer progression. The remodelling of calcium (Ca2+) signalling and the role of the Ca2+ signal in controlling key events in cancer cells such as proliferation, invasion and the acquisition of resistance to cell death pathways is well established. Most of the work defining such changes has focused on Ca2+ permeable Transient Receptor Potential (TRP) Channels and some voltage gated Ca2+ channels. However, the identification of ORAI channels, a little more than a decade ago, has added a new dimension to how a Ca2+ influx pathway can be remodelled in some cancers and also how calcium signalling could contribute to tumour progression. ORAI Ca2+ channels are now an exemplar for how changes in the expression of specific isoforms of a Ca2+ channel component can occur in cancer, and how such changes can vary between cancer types (e.g. breast cancer versus prostate cancer), and even subtypes (e.g. oestrogen receptor positive versus oestrogen receptor negative breast cancers). ORAI channels and store operated Ca2+ entry are also highlighting the diverse roles of Ca2+ influx pathways in events such as the growth and metastasis of cancers, the development of therapeutic resistance and the contribution of tumour microenvironmental factors in cancer progression. In this review we will highlight some of the studies that have provided evidence for the need to deepen our understanding of ORAI Ca2+ channels in cancer. Many of these studies have also suggested new ways on how we can exploit the role of ORAI channels in cancer relevant processes to develop or inform new therapeutic strategies.
ORAI1  Cancer  invasion  drug_resistance  Review 
may 2019 by Segalllab
Myoepithelial cells are a dynamic barrier to epithelial dissemination | JCB
The mammary epithelium is composed of an inner luminal and surrounding myoepithelial cell layer. The presence of cancer cells beyond the myoepithelium defines invasive breast cancer, yet the role of the myoepithelium during invasion remains unclear. We developed a 3D organotypic culture assay to model this process through lineage-specific expression of the prometastatic transcription factor Twist1. We sought to distinguish the functional role of the myoepithelium in regulating invasion and local dissemination. Myoepithelial-specific Twist1 expression induced cell-autonomous myoepithelial cell escape. Remarkably, luminal-specific Twist1 expression was rarely sufficient for escape. Time-lapse microscopy revealed that myoepithelial cells collectively restrain and reinternalize invading Twist1+ luminal cells. Barrier function correlated with myoepithelial abundance and required the expression of α-smooth muscle actin and P-cadherin. We next demonstrated that myoepithelial cells can restrain and recapture invasive cancer cells. Our data establish the concept of the myoepithelium as a dynamic barrier to luminal dissemination and implicate both smooth muscle contractility and intercellular adhesion in barrier function.
myoepithelial_cells  invasion  twist  luminal_cells 
april 2019 by Segalllab
TMEM106B drives lung cancer metastasis by inducing TFEB -dependent lysosome synthesis and secretion of cathepsins | Nature Communications
Mechanism for lysosmal secretion of cathepsins to stimulate lung cancer

Metastatic lung cancer is the leading cause of cancer-associated mortality worldwide, therefore necessitating novel approaches to identify specific genetic drivers for lung cancer progression and metastasis. We recently performed an in vivo gain-of-function genetic screen to identify driver genes of lung cancer metastasis. In the study reported here, we identify TMEM106B as a primary robust driver of lung cancer metastasis. Ectopic expression of TMEM106B could significantly promote the synthesis of enlarged vesicular lysosomes that are laden with elevated levels of active cathepsins. In a TFEB-dependent manner, TMEM106B could modulate the expression of lysosomal genes of the coordinated lysosomal expression and regulation (CLEAR) pathway in lung cancer cells and patient samples. We also demonstrate that TMEM106B-induced lysosomes undergo calcium-dependent exocytosis, thereby releasing active lysosomal cathepsins necessary for TMEM106B-mediated cancer cell invasion and metastasis in vivo, which could be therapeutically prevented by pharmacological inhibition of cathepsins. Further, in TCGA LUAD data sets, 19% of patients show elevated expression of TMEM106B, which predicts for poor disease-free and overall-survival.
cathepsins  lysosomes  calcium  invasion  Cancer 
april 2019 by Segalllab
p38-mediated phosphorylation at T367 induces EZH2 cytoplasmic localization to promote breast cancer metastasis | Nature Communications
Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. Here we show that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. p38-mediated EZH2 phosphorylation at T367 promotes EZH2 cytoplasmic localization and potentiates EZH2 binding to vinculin and other cytoskeletal regulators of cell migration and invasion. Ectopic expression of a phospho-deficient T367A-EZH2 mutant is sufficient to inhibit EZH2 cytoplasmic expression, disrupt binding to cytoskeletal regulators, and reduce EZH2-mediated adhesion, migration, invasion, and development of spontaneous metastasis. These results point to a PRC2-independent non-canonical mechanism of EZH2 pro-metastatic function.
ezh2  polycomb  invasion  vinculin  p38 
april 2019 by Segalllab
Wogonin suppresses the LPS-enhanced invasiveness of MDA-MB-231 breast cancer cells by inhibiting the 5-LO/BLT2 cascade
Interesting that TLR4 is on 231 cells and can enhance invasion with LPS through leukotrien B4 receptor 2 (probably other stuff as well).

Recent studies have demonstrated that following exposure to lipopolysaccharide (LPS) in vitro and in vivo, cancer cells become more aggressive as a result of the stimulation of the toll-like receptor 4 (TLR4)/myeloid differentiation primary response 88 (MyD88) pathway (8-10). In particular, LPS-induced TLR4 overexpression in breast cancer tissues is associated with lymph node metastasis (11,12). A previous study has demonstrated that LPS upregulates the MyD88/5-lipoxygenase (5-LO)/BLT2 cascade and that BLT2 depletion attenuates the ability of LPS to induce invasiveness and interleukin-8 (IL-8) biosynthesis in aggressive breast cancer cells. In addition, BLT2 inhibition reduces the incidence of LPS-induced metastasis in an in vivo breast cancer mouse model (13). On the basis of this information, pharmaceutical or natural agents that directly interfere with the production of BLT2, or antagonize its signaling functions, may be effective in attenuating breast cancer progression.
231_cells  TLRs  tlr4  lps  invasion 
april 2019 by Segalllab
Arf6-driven cell invasion is intrinsically linked to TRAK1-mediated mitochondrial anterograde trafficking to avoid oxidative catastrophe | Nature Communications
Regulation of mitochondrial movmeent in 231 cells affects invasion and ROS

Mitochondria dynamically alter their subcellular localization during cell movement, although the underlying mechanisms remain largely elusive. The small GTPase Arf6 and its signaling pathway involving AMAP1 promote cell invasion via integrin recycling. Here we show that the Arf6–AMAP1 pathway promote the anterograde trafficking of mitochondria. Blocking the Arf6-based pathway causes mitochondrial aggregation near the microtubule-organizing center, and subsequently induces detrimental reactive oxygen species (ROS) production, likely via a mitochondrial ROS-induced ROS release-like mechanism. The Arf6-based pathway promotes the localization of ILK to focal adhesions to block RhoT1–TRAK2 association, which controls mitochondrial retrograde trafficking. Blockade of the RhoT1–TRAK1 machinery, rather than RhoT1–TRAK2, impairs cell invasion, but not two-dimensional random cell migration. Weakly or non-invasive cells do not notably express TRAK proteins, whereas they clearly express their mRNAs. Our results identified a novel association between cell movement and mitochondrial dynamics, which is specific to invasion and is necessary for avoiding detrimental ROS production.
ROS  231_cells  arf6  mitochondria  invasion 
march 2019 by Segalllab
Northern Territory Intervention (2007)
then prime minister, John Howard, and his Indigenous affairs minister, Mal Brough, launched the Northern Territory Emergency Response (NTER) into remote Indigenous communities.

With no warning, and no consultation, the federal government moved swiftly to seize control of many aspects of the daily lives of residents in 73 targeted remote communities. It implemented coercive measures that would have been unthinkable in non-Indigenous communities.

By deploying uniformed members of the Australian Defence Forces into the communities to establish logistics, the Intervention was designed to send a clear message of disruption and control. The government’s suspension of the Racial Discrimination Act raised further cause for concern.

Township leases were compulsorily acquired over Aboriginal-owned land by the Commonwealth for a five-year period. And the permit system administered by Aboriginal land councils to control access to Aboriginal land was revoked.

Medical teams were flown in to conduct compulsory health checks on children. Signs were posted declaring bans on alcohol and pornography in township areas.

Income management was applied to all community residents receiving welfare payments, and income support payments were linked to satisfactory school attendance.

The successful Community Development Employment Projects program was abolished, and employees were forced onto unemployment benefits. The police presence was increased in prescribed communities. And customary law was no longer allowed to be considered in bail applications and sentencing in criminal court cases.
Australia  Invasion  racism  NT  NTER  ADF  RDA  John-Howard  Indigenous-affairs  Human-rights2007  2017 
march 2019 by zzkt
Rab34 regulates adhesion, migration, and invasion of breast cancer cells | Oncogene
Rab34 is up in 231, 549 cells and gets phoshoryated upon plating and is involved in integrin b3 dynamics.

The small GTPase Rab34 regulates spatial distribution of the lysosomes, secretion, and macropinocytosis. In this study, we found that Rab34 is over-expressed in aggressive breast cancer cells, implying a potential role of Rab34 in breast cancer. Silencing Rab34 by shRNA inhibits cell migration, invasion, and adhesion of breast cancer cells. Rab34 specifically binds to the cytoplasmic tail of integrin β3, and depletion of Rab34 promotes the degradation of integrin β3. Interestingly, EGF induces the translocation of Rab34 to the membrane ruffle, which is greatly enhanced by the expression of Src kinase. Accordingly, Rab34 is tyrosine phosphorylated by Src at Y247 residue. A mutant mimicking phosphorylated form of Rab34 (Rab34Y247D) promotes cell migration and invasion. Importantly, the tyrosine phosphorylation of Rab34 is inhibited in cells in suspension, and increased with the cells re-adhesion. In addition, Rab34Y247D promotes cell adhesion, and enhances integrin β3 endocytosis and recycling. The results uncover a role of Rab34 in migration and invasion of breast cancer cells and its involvement in cancer metastasis, and provide a novel mechanism of tyrosine phosphorylation of Rab34 in regulating cell migration, invasion, and adhesion through modulating the endocytosis, stability, and recycling of integrin β3.
231_cells  BT474  Integrins  itgb3  invasion  Metastasis  Src  adhesion 
march 2019 by Segalllab
Human Kallikrein 6 Degrades Extracellular Matrix Proteins and May Enhance the Metastatic Potential of Tumour Cells - Abstract - Tumor Biology 2004, Vol. 25, No. 4 - Karger Publishers
Human kallikrein 6 (hK6), a trypsin-like serine protease, is a newly identified member of the kallikrein gene family. Its involvement in inflammatory CNS lesions and in demyelination has been reported. Recent work has suggested that expression of this enzyme is significantly elevated in patients with ovarian cancer. We have identified many tumour cell lines that secrete hK6, but its physiological role is unknown. Here, we try to unveil the role of this kallikrein in the metastasis and invasion of tumour cells. We demonstrate that purified human recombinant hK6 can cleave gelatin in zymography and can efficiently degrade high-molecular-weight extracellular matrix proteins such as fibronectin, laminin, vitronectin and collagen. In Boyden chamber assays, we found that tumour cells treated with a neutralizing hK6 antibody migrate less than control cells. We conclude that hK6 might play a role in the invasion and metastasis of tumour cells and may be a candidate therapeutic target.
klk6  invasion  degradation 
march 2019 by Segalllab
BRD4 regulates breast cancer dissemination through Jagged1/Notch1 signaling
in 231 and sum149, BRD4 is required for jag1 expression (also IL6 induced invasion)

The Bromodomain and ExtraTerminal (BET) proteins are epigenetic ‘readers’ of acetylated histones in chromatin and have been identified as promising therapeutic targets in diverse cancers. However, it remains unclear how individual family members participate in cancer progression, and small molecule inhibitors such as JQ1 can target functionally independent BET proteins. Here we report a signaling pathway involving BRD4 and the ligand/receptor pair Jagged1/Notch1 that sustains triple-negative breast cancer migration and invasion. BRD4, but not BRD2 or BRD3, regulated Jagged1 expression and Notch1 signaling. BRD4-selective knockdown suppressed Notch1 activity and impeded breast cancer migration and invasion. BRD4 was required for interleukin-6-stimulated, Notch1-induced migration and invasion, coupling microenvironment inflammation with cancer propagation. Moreover, in patients, BRD4 and Jagged1 expression positively correlated with the presence of distant metastases. These results identify a BRD4/Jagged1/Notch1 signaling pathway that is critical for dissemination of triple-negative breast cancer.
sum149  231_cells  JAG1  Notch1  invasion  brd4 
february 2019 by Segalllab

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