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Ether lipids influence cancer cell fate by modulating iron uptake

The contribution of ether lipid species in cancer cell fate has not been fully understood yet. Here the authors show that malignant cancer cells employ ether lipids to modulate membrane biophysical properties, enhancing iron endocytosis and ferroptosis susceptibility.

Ryan P. Mansell
Sebastian Müller
Whitney S. Henry
ResearchOpen Access27 Jan 2026
Nature Communications

P: 1-19
Addendum: A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages

Haihui Lu
Karl R. Clauser
Robert A. Weinberg
Amendments and Corrections27 Nov 2015
Nature Cell Biology

Volume: 17, P: 1607
Genome-wide CRISPR screen identifies PRC2 and KMT2D-COMPASS as regulators of distinct EMT trajectories that contribute differentially to metastasis

Through genome-wide and focused CRISPR screens, Zhang et al. discover that loss of PRC2 or KMT2D-COMPASS enables distinct EMT trajectories, which exert differential effects on the metastatic capability of carcinoma cells.

Yun Zhang
Joana Liu Donaher
Robert A. Weinberg
Research11 Apr 2022
Nature Cell Biology

Volume: 24, P: 554-564
Plasticity of ether lipids promotes ferroptosis susceptibility and evasion

The cellular organelles peroxisomes contribute to the sensitivity of cells to ferroptosis by synthesizing polyunsaturated ether phospholipids, and changes in the abundances of these lipids are associated with altered sensitivity to ferroptosis during cell-state transitions.

Yilong Zou
Whitney S. Henry
Stuart L. Schreiber
Research16 Sept 2020
Nature

Volume: 585, P: 603-608
IL-1β inflammatory response driven by primary breast cancer prevents metastasis-initiating cell colonization

Castaño et al. show that primary breast tumours drive an IL-1β -mediated inflammatory response that inhibits cellular plasticity and metastatic colonization of metastasis-initiating cells.

Zafira Castaño
Beatriz P. San Juan
Sandra S. McAllister
Research27 Aug 2018
Nature Cell Biology

Volume: 20, P: 1084-1097
Therapeutic silencing of miR-10b inhibits metastasis in a mouse mammary tumor model

Efforts to develop drugs that would prevent a primary tumor from spreading to new sites have been hampered by a lack of metastasis-specific targets. Working with a mouse model of breast cancer, Ma et al. show for the first time that metastasis formation can be substantially reduced by inhibition of a pro-metastatic microRNA.

Li Ma
Ferenc Reinhardt
Robert A Weinberg
Research28 Mar 2010
Nature Biotechnology

Volume: 28, P: 341-347
Cancer-specific PERK signaling drives invasion and metastasis through CREB3L1

PERK stress signaling is an important driver of cancer invasion and metastasis, but chemical inhibitors of PERK cause side effects. Here, the authors find that CREB3L1 is required for PERK's pro-metastatic function in breast cancer, and its inhibition suppresses cancer invasion and metastasis.

Yu-Xiong Feng
Dexter X. Jin
Piyush B. Gupta
ResearchOpen Access20 Oct 2017
Nature Communications

Volume: 8, P: 1-10
LACTB is a tumour suppressor that modulates lipid metabolism and cell state

LACTB modulates mitochondrial lipid metabolism and changes the differentiation state of breast cancer cells, thereby negatively affecting the growth of various tumorigenic, but not non-tumorigenic, cells both in vitro and in vivo.

Zuzana Keckesova
Joana Liu Donaher
Robert A. Weinberg
Research22 Mar 2017
Nature

Volume: 543, P: 681-686
A breast cancer stem cell niche supported by juxtacrine signalling from monocytes and macrophages

Weinberg and colleagues report that monocytes and macrophages interact with stem-like human mammary epithelial cells to create a breast cancer stem cell niche.

Haihui Lu
Karl R. Clauser
Robert A. Weinberg
Research28 Sept 2014
Nature Cell Biology

Volume: 16, P: 1105-1117
miR-9, a MYC/MYCN-activated microRNA, regulates E-cadherin and cancer metastasis

miRNAs can both promote and repress tumorigenesis, and directly control epithelial–mesenchymal transition (EMT). miR-9 (which is upregulated in breast cancer cells) is activated by MYC and MYCN, and regulates EMT and metastasis through direct control of E-cadherin. In contrast, tumour angiogenesis is controlled indirectly through effects on vascular endothelial growth factor (VEGF) expression.

Li Ma
Jennifer Young
Robert A. Weinberg
Research21 Feb 2010
Nature Cell Biology

Volume: 12, P: 247-256
Distinct EMT programs control normal mammary stem cells and tumour-initiating cells

This study finds that the epithelial-to-mesenchymal (EMT) transition program, which is common to both mammary gland reconstituting stem cells and mammary tumour-initiating cells, is differentially regulated by two distinct EMT factors, Slug and Snail; the findings illustrate that although they appear similar, normal tissue stem cells and tumour-initiating cells are controlled by distinct regulatory processes.

Xin Ye
Wai Leong Tam
Robert A. Weinberg
Research02 Sept 2015
Nature

Volume: 525, P: 256-260

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