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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_FAP_KPCScr_and_miR-27a-KD]

ABSTRACT: The study aims to understand if modulating miR-27a-3p reduces tumor burden and alleviates muscle wasting and FAP dysregulation using an experimental model of pancreatic cancer cachexia. KPCY- a murine pancreatic cancer cell line was utilized for the study.

ORGANISM(S): Mus musculus

PROVIDER: GSE256322 | GEO | 2026/08/10

REPOSITORIES: GEO

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_KPC_KPCScr_and_miR-27a-KD]

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_FAP_KPCScr_and_miR-27a-KD]

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_KPC_KPCScr_and_miR-27a-KD]

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [snRNASeq_whole_muscle]

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_FAP_timeseries]

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia

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Neural invasion induces cachexia via astrocytic activation of neural route in pancreatic cancer

Project description:Pancreatic cancer is characterized by a high frequency of cachexia, pain and neural invasion (N-inv). Neural damage is occurred by N-inv and modulates pain and muscle atrophy via the activation of astrocyte in the connected spine. The activated astrocyte by N-inv, thus, may affect cachexia in pancreatic cancer. Clinical studies in patients and autopsy cases with pancreatic cancer have revealed that N-inv is related to cachexia and astrocytic activation. We established a novel murine model of cancer cachexia using N-inv of human pancreatic cancer cells. Mice with N-inv showed a loss of body weight, skeletal muscle, and fat mass without appetite loss, which are compatible with an animal model of cancer cachexia. Activation of astrocytes in the spinal cord connected with N-inv was observed in our model. Experimental cachexia was suppressed by disrupting neural routes or inhibiting the activation of astrocytes. These data provide the first evidence that N-inv induces cachexia via astrocytic activation of neural route in pancreatic cancer. We produced neural invasion (N-inv) model using intraneural injection of Capan-1 cells to left sciatic nerve of male SCID mouse. For controls, subcutaneous model (SC) and PBS model were produced. Microarray analysis was performed using the first lumbar cord (L1) from PBS, SC, and N-inv mice at 6 w (n = 2 each).

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Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_FAP_timeseries]

Project description:Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [RNASeq_FAP_timeseries]

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Project description:Characterizing the role of fibroadipogenic progenitor in experimental model of pancreatic cancer cachexia [snRNASeq_whole_muscle]

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Project description:Pancreatic β-cell dysfunction caused by obesity can be associated with alterations in the levels of microRNAs (miRNAs). However, the role of miRNAs in such processes remains elusive. Here, we show that pancreatic islet miR-27a-5p, which is markedly increased in obese mice and impairs insulin secretion, is mainly delivered by visceral adipocyte-derived extracellular vesicles (EVs). Depleting miR-27a-5p significantly improves insulin secretion and glucose intolerance in db/db mice. Supporting the function of EVs’ miR-27a-5p as a key pathogenic factor, intravenous injection of miR-27a-5p-containing EVs shows their distribution in mouse pancreatic islets. Tracing the injected AAV-miR-27a-5p (AAV-miR-27a) or AAV-FABP4-miR-27a-5p (AAV-FABP4-miR-27a) in visceral fat results in upregulating miR-27a-5p in EVs and serum, and elicits mouse pancreatic β-cell dysfunction. Mechanistically, miR-27a-5p directly targets L-type Ca2+ channel subtype CaV1.2 (Cacna1c) and reduces insulin secretion in β-cells. Overexpressing mouse CaV1.2 largely abolishes the insulin secretion injury induced by miR-27a-5p. These findings reveal a causative role of EVs’ miR-27a-5p in visceral adipocyte-mediated pancreatic β-cell dysfunction in obesity-associated type 2 diabetes mellitus.

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