Yuanting Lu's research while affiliated with Guangzhou Medical University and other places
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Publications (13)
A correction to this paper has been published: https://doi.org/10.1038/s41419-021-03420-5
Abstract Cancer-associated fibroblasts (CAFs), a dominant component of the pancreatic tumor microenvironment, are mainly considered as promotors of malignant progression, but the underlying molecular mechanism remains unclear. Here, we show that SDF-1 secreted by CAFs stimulates malignant progression and gemcitabine resistance in pancreatic cancer,...
Repairing articular cartilage defects is difficult due to the hypovascular biostructure and poor self-repairing capacity of articular cartilage. Currently, mesenchymal stem cells (MSCs) with excellent differentiation potential are considered as a promising biological approach for cartilage regeneration. The effect, however, remains far from satisfa...
Citations
... For example, anti-PD-L1 immunotherapy resistance was correlated with increased levels of LRRC15 + CAFs [14], and CAFs expressing fibroblast activation protein marker in an immunosuppressive environment were linked to immunotherapy failure [15]. SDF-1-secreting CAFs mediated SATB-1 overexpression and gemcitabine resistance in pancreatic cancer [16], and hepatocyte growth factor-secreting CAFs mediated tyrosine kinase resistance in triple-negative breast cancer through paracrine activation, while neuregulin 1-secreting CAFs promoted antiandrogen resistance in prostate cancer by activating HER3 [17,18]. Human ovarian cancer cells can activate fibroblasts by releasing EVs, causing the surrounding cells to enter a CAF-like state [19]. ...
... In a study, treatment of MSCs with a combination of IONPs and hypoxia exerted synergistic effects. It improved MSC migration and chondrogenic differentiation in-vitro and demonstrated corresponding remedial effects in-vivo [131]. ...
... The desmoplastic stroma and hypoxic environment have also been reported to promote EMT and cause gemcitabine resistance [96,97]. Accumulated evidence has revealed that desmoplastic stroma simply does not develop a physical barrier to gemcitabine; moreover, the respective components in the TME act to resist gemcitabine [98][99][100][101]. ...
