How does cancer cell metabolism affect tumor migration and invasion?

Han, Tianyu; Kang, De; Ji, Daokun; Wang, Xiaoyu; Zhan, Weihua; Fu, Minggui; Xin, Hong‐Bo; Wang, Jianbin

doi:10.4161/cam.26345

Cited by 179 publications

(163 citation statements)

References 104 publications

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“…Lastly, the expression of GLUT3 is induced during EMT to support increased glucose consumption in mesenchymal cells [109]. Indeed, tumor cell migration and invasion seem to be supported by specific metabolic programs [110]. Together, these findings lend support to the notion that regulation of metabolic genes by the ERRs may contribute to ERRdependent EMT/MET, migration, and invasion.…”

Section: Coordination Of Err-driven Metabolism In Cancer Progressionmentioning

confidence: 85%

There and back again: The journey of the estrogen-related receptors in the cancer realm

Tam

Giguère

2016

The Journal of Steroid Biochemistry and Molecular Biology

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Section: Coordination Of Err-driven Metabolism In Cancer Progressionmentioning

confidence: 85%

There and back again: The journey of the estrogen-related receptors in the cancer realm

Tam

Giguère

2016

The Journal of Steroid Biochemistry and Molecular Biology

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“…Cancer metabolism is known to affect cell migration (44). CHCHD2 was implicated as a regulator of oxphos (20), and Dependence of mitochondrial respiration on CHCHD2 protein expression.…”

Section: Discussionmentioning

confidence: 99%

CHCHD2 Is Coamplified with EGFR in NSCLC and Regulates Mitochondrial Function and Cell Migration

Wei

Vellanki

Coyaud

et al. 2015

Molecular Cancer Research

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Coiled-coil-helix-coiled-coil-helix domain-containing 2, a mitochondrial protein, encoded by CHCHD2 is located at chromosome 7p11.2 and proximal to the EGFR gene. Here, bioinformatic analyses revealed that CHCHD2 is consistently coamplified with EGFR in non-small cell lung carcinoma (NSCLC). In addition, CHCHD2 and EGFR protein expression levels were positively correlated and upregulated relative to normal lung in NSCLC tumor-derived xenografts. Knockdown of CHCHD2 expression in NSCLC cells attenuated cell proliferation, migration, and mitochondrial respiration. CHCHD2 protein-protein interactions were assessed by the complementary approaches of affinity purification mass spectrometry and in vivo proximity ligation. The CHCHD2 interactome includes the apparent hub proteins C1QBP (a mitochondrial protein) and YBX1 (an oncogenic transcription factor), and an overlapping set of hub-associated proteins implicated in cell regulation.Implications: CHCHD2 influences mitochondrial and nuclear functions and contributes to the cancer phenotype associated with 7p11.2 amplification in NSCLC. Mol Cancer Res; 13(7); 1119-29. Ó2015 AACR.

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“…Cancer cells exposed to hypoxia, both in vitro and in vivo, undergo genetic and/or phenotypic changes that influence cellular metabolism, proliferation, and development of radio/chemo-resistance (3)(4)(5)(6). These changes allow the cells to survive in stressful environments.…”

Section: Introductionmentioning

confidence: 99%

A paper-based invasion assay: Assessing chemotaxis of cancer cells in gradients of oxygen

et al. 2015

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This work describes a 3D, paper-based assay that can isolate subpopulations of cells based on their invasiveness (i.e., distance migrated in a hydrogel) in a gradient of concentration of oxygen (O 2 ). Layers of paper impregnated with a cell-compatible hydrogel are stacked and placed in a plastic holder to form the invasion assay. Stacking the layers of paper assembles them into 3D tissue-like constructs of defined thickness and composition. The plastic holder ensures the layers of paper are in conformal contact; this geometry allows the cells to migrate between adjacent layers through the embedded hydrogel. In most assays, the stack comprises a single layer of paper containing mammalian cells suspended in a hydrogel, sandwiched between multiple layers of paper containing only hydrogel (into which the cells migrate). Cells in the stack consume and produce small molecules; these molecules diffuse throughout the stack to generate gradients both in the stack, and between the stack and the bulk culture medium. Placing the cell-containing layer in different positions of the stack, or modifying the permeability of the holder to oxygen or proteins, alters the profile of the gradients within the stack. Physically separating the layers after culture isolates subpopulations of cells that migrated different distances, and enables their subsequent analysis or culture. Using this system, three independent cell lines derived from A549 cancer cells are shown to produce distinguishable migration behavior in a gradient of oxygen. This result is the first experimental demonstration that oxygen acts as a chemoattractant for cancer cells. Page 3 of 35 Significance StatementThe invasion of cancerous cells from a tumor into surrounding tissues is one contribution to metastasis-a major contributor to death for patients with cancer. There is a strong link between the directed invasion of cancer cells and the gradients of molecules formed in the microenvironment of the tumor. Using a paper-based invasion assay, this work demonstrates that oxygen-a nutrient known to induce significant behavioral changes to cells within a tumor in a concentration-dependent manner-can also act as a chemoattractant, resulting in the migration of cancer cells towards higher concentrations of oxygen. This finding, and the invasion assay described, could lead to a better understanding of oxygen-based chemotaxis in cancer, and ultimately new strategies for managing metastasis.

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How does cancer cell metabolism affect tumor migration and invasion?

Cited by 179 publications

References 104 publications

There and back again: The journey of the estrogen-related receptors in the cancer realm

There and back again: The journey of the estrogen-related receptors in the cancer realm

CHCHD2 Is Coamplified with EGFR in NSCLC and Regulates Mitochondrial Function and Cell Migration

A paper-based invasion assay: Assessing chemotaxis of cancer cells in gradients of oxygen

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