NEUROG3 (Neurogenin 3)

A transient pulse of NEUROG3 repressed luminal identity and activated neuroendocrine programs, producing neuroendocrine cells within seven days. In summary, our findings identify NEUROG3 as a potential mediator of prostate cancer progression and establish a rapid in vitro model in which its transient activation is sufficient to initiate neuroendocrine differentiation.

Our findings demonstrate that pancreatic cancer cells can be induced to transdifferentiate through NeuroD1 activation or pharmacological induction, suggesting a potential therapeutic strategy to mitigate malignancy by reprogramming tumor cells into less aggressive states.

Clinically, DNES-derived neoplasms span multiple organs, produce diverse hormonal syndromes, and are managed with somatostatin analogues, epigenetic drugs, and emerging immunotherapies. Recognizing DNES as a diffuse, integrative regulatory network clarifies mechanisms of chronic inflammation and cancer evolution and offers novel therapeutic entry points for disorders ranging from asthma to pancreatic neuroendocrine carcinomas.

T1D-iPSCs derived from T1D-PBMCs can be differentiated into insulin+ β-like cells, albeit with functional immaturity. These cells represent a potential source of seed cells for β-cell replacement therapy in T1D.

Harmol and ligandrol improved glucose tolerance in diabetic male rats induced by a high-fat diet and streptozotocin. Our results suggest that harmol could serve as a novel anti-diabetic agent for T2DM with a unique mechanism that targets AR for β-cell revival and enhances glucose tolerance.

Ginger extract exerts an antidiabetic effect by acting on pancreatic progenitors and α-cells to restore β-cell mass in STZ-induced diabetic rats. These findings suggest that ginger extract could be a potential stimulator of β-cell neogenesis, which provides an alternative to meet the increasing demand for exogenous insulin in patients with diabetes.

GE induces β-cell neogenesis in DRs and restores islet architecture. The newly formed mature β-like cells could have originated through the differentiation of endocrine progenitor cells as well as α- to β-cell transdifferentiation.

EA could lower the blood glucose levels in T2DM rats, alleviate chronic inflammatory responses in the islets, and improve the dedifferentiation of pancreatic β-cells, which may be related to the inhibition of pancreatic NF-κB pathway expression.

Our findings reveal the effectiveness of N-Ad-MSCs in differentiating into IPCs in vitro and controlling the hyperglycemia of STZ-induced diabetic rats in vivo compared to DM-Ad-MSCs.

MDCH has therapeutic effects on T2D, through regulating the SIRT1/FOXO1 signalling pathway to inhibit pancreatic β-cell dedifferentiation, which has not been reported previously.

In conclusion, our data demonstrated significant beneficial actions of cotadutide in DIO mice, such as weight loss, glycemic control, and insulin resistance improvement. In addition, cotadutide counteracted the pathological adaptive cellular arrangement of the pancreatic islet in obese mice, improving the markers of the transdifferentiating pathway, proliferation, apoptosis, and ER stress.

FTZ can restore the insulin-secreting function of the impaired pancreatic islet, improve blood glucose level, possibly via the enhancing β cell regeneration via upregulation of PDX-1, MAFA, and NGN3 in T1DM mice, and may be a potential therapeutic drug for T1DM.