L.-E. Quek

Macropinocytosis mediates resistance to loss of glutamine transport in triple-negative breast cancer

The paper shows that TNBC cells compensate for loss of ASCT2 glutamine uptake by increasing macropinocytosis, suggesting resistance to targeting glutamine transport alone.

Pathway metabolite ratios reveal distinctive glutamine metabolism in a subset of proliferating cells

The paper identifies distinct glutamine metabolism in a subset of proliferating cells using pathway-centric metabolomic analysis of cancer and non-cancer cell lines.

CPT1a regulates the delivery of extracellular fatty acids for cardiolipin turnover in prostate cancer cells.

The paper shows that CPT1a regulates the uptake of extracellular fatty acids into mitochondria for cardiolipin remodeling in prostate cancer cells, despite these fatty acids being minor contributors to the TCA cycle.

ACSM1 and ACSM3 regulate prostate cancer fatty acid metabolism to promote tumour growth and constrain ferroptosis

This study identifies ACSM1 and ACSM3 as AR-regulated factors that promote prostate cancer growth by enhancing fatty acid metabolism and suppressing ferroptosis.

Insulin sensitivity is preserved in mice made obese by feeding a high starch diet

This study shows that mice fed a high starch diet become obese but remain insulin sensitive, unlike those on a high fat diet, with differences in ceramide levels and lipogenesis contributing to this effect.

Nicotinamide mononucleotide (NMN) de-amidation by host-microbiome interactions

This study shows orally delivered NMN undergoes deamidation and incorporation into mammalian tissue via the de novo pathway, with microbiome disruption reducing this process and increasing gut NAD+ availability.

A feedback loop between the androgen receptor and 6-phosphogluoconate dehydrogenase (6PGD) drives prostate cancer growth

This study identifies a feedback loop between the androgen receptor and 6PGD that drives prostate cancer growth and shows that targeting both improves therapeutic efficacy.

EXERCISE-INDUCED BENEFITS ON GLUCOSE HANDLING IN A MODEL OF DIET-INDUCED OBESITY ARE REDUCED BY CONCURRENT NICOTINAMIDE MONONUCLEOTIDE

This study shows that nicotinamide mononucleotide (NMN) treatment reduces the beneficial effects of exercise on glucose handling in diet-induced obese mice, likely due to altered redox metabolism.