Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression analysis of patient-derived engineered organoid model of thyroid cancer (TC)

ABSTRACT: Inter-tumor heterogeneity is a major hurdle in thyroid cancer (TC) precision therapy. The use of non-engineered organoids (NEOs), derived from primary tissue, as a potent tool for cancer drug screening is limited by their dependence on inefficient manual procedures. Here, we establish droplet-engineered organoids (DEOs) derived from TC patients using microfluidic technology, which recapitulates histopathology and genomic landscape of parental tumors, and preserve the drug sensitivity differences of patients. Furthermore, we reveal NF-κB pathway as a major mediator of advanced DEOs generation. A NF-κB inhibitor and anti cancer drugs are screened, exhibiting a marked anti-proliferative effect. Together, our study demonstrates a microfluidic-based approach for rapid construction of TC DEOs and investigates the maturation mechanisms, providing an ideal in vitro model and novel insights for the development of therapeutic strategies against thyroid carcinoma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE296099 | GEO | 2025/12/31

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcriptome of thyroid cancer (TC) cells after coculture with TC-induced macrophages

Project description:Transcriptome of thyroid cancer (TC) cells after coculture with TC-induced macrophages

| PRJNA493059 | ENA

Gene expression analysis of patient-derived engineered organoid model of thyroid cancer (TC)

Project description:Gene expression analysis of patient-derived engineered organoid model of thyroid cancer (TC)

| PRJNA1257792 | ENA

Establishment of a human tongue cancer organoid biobank enables early diagnosis, prognosis, and identification of therapeutic targets

Project description:Tongue cancer (TC) is the most frequent and a serious type of oral cancer with major clinical challenges such as lymph node metastasis and the appearance of chemotherapy resistant cells. Thus, development of diagnostic and therapeutic strategies to target these malignant cancer cells is urgently required. Here, we describe a novel and highly efficient method to generate human TC organoids, thereby creating a TC organoid biobank with primary and metastatic TC from 28 patients with diverse ages and cancer stages. These organoid lines can be expanded, passed, stored frozen for long periods, and they can reproduce original TC tissues in vitro and in xenograft models. The organoids showed different properties among patients with respect to the proliferation capacity and susceptibility to cisplatin, a commonly used chemotherapeutic agent in TC therapy. This suggests that TC organoids are useful for accurate risk grading and predicting the prognosis at early stages of TC, which is difficult to diagnose clinically. Thus, human TC organoids are useful for profiling TCs, which will lead to drug development against metastatic and chemotherapy-resistant TCs.

2024-09-13 | GSE145057 | GEO

Escovopsis sp. TC strain:TC

Project description:Escovopsis sp. TC strain:TC Genome sequencing and assembly

| PRJNA388866 | ENA

Alicyclobacillus sp. TC strain:TC

Project description:Alicyclobacillus sp. TC strain:TC Genome sequencing and assembly

| PRJNA562382 | ENA

A flow-enhanced microphysiological model of the human thyroid elicits a more organotypic response to endocrine disruptors

Project description:In this study, we aimed to engineer an in vitro model that better resembles the glandular architecture and hemodynamic perfusion of the native thyroid than current in vitro models, and that can better evaluate the effect of potential endocrine disrupting chemicals (EDCs) on the thyroid. We constructed a human thyroid-on-a-chip (ThyO) model by culturing NKX2-1wt-GFP/PAX8 human embryonic stem cell-derived thyroid organoids in an in-house developed microfluidic system for 7 days. We then performed fluorescence-activated cell sorting (FACS) of NKX2-1+ cells. We compared our ThyO model to static organoid controls using RNA sequencing. In addition, we mechanistically elucidated the effect of 7 days exposure to the EDC benzo(k)fluoranthene (BkF) on thyroid physiology both in the ThyO chip model and static organoids.

2024-12-07 | E-MTAB-13637 | biostudies-arrayexpress

Transcriptome of thyroid cancer (TC) cells after coculture with TC-induced macrophages

Project description:RNA sequencing data of TPC-1 cells (TC cell line) after co-culture with TC-induced macrophages. We used an in vitro co-culture model of a human TC cell line, TPC1 (RET/PTC rearrangement), and human primary monocytes.

2020-09-21 | GSE120391 | GEO

Enterococcus sp. E843-TC isolate:E843-TC

Project description:Enterococcus sp. E843-TC isolate:E843-TC Genome sequencing

| PRJNA755459 | ENA

Genome wide chromatin changes in TC-32 and TC-71 Ewing sarcoma cell lines.

Project description:We performed ChIPseq on histone modification marks, transcriptional factors and chromatin architectural proteins in TC-32 and TC-71 Ewing sarcoma cell lines.

2019-08-07 | GSE115250 | GEO

Ribosomal protein S3 mediates drug resistance of proteasome inhibitor: therapeutic application in multiple myeloma

Project description:Multiple myeloma (MM) remains incurable due to drug resistance. Ribosomal protein S3 (RPS3) has been identified as a non-Rel subunit of NF-κB. However, the detailed biological roles of RPS3 remain unclear. Here, we report for the first time that RPS3 is necessary for MM survival and drug resistance. RPS3 was highly expressed in MM, and knockout of RPS3 in MM inhibited cell growth and induced cell apoptosis both in vitro and in vivo. Overexpression of RPS3 mediated the proteasome inhibitor resistance of MM and delayed the survival of MM tumour-bearing animals. Moreover, our present study found an interaction between RPS3 and the thyroid hormone receptor interactor 13 (TRIP13), an oncogene related to MM tumorigenesis and drug resistance. We demonstrated that the phosphorylation of RPS3 was mediated by TRIP13 via PKCδ, which played an important role in activating the canonical NF-κB signalling and inducing cell survival and drug resistance in MM. Notably, the inhibition of NF-κB signalling by the small-molecule inhibitor targeting TRIP13, DCZ0415, was capable of triggering synergistic cytotoxicity when combined with bortezomib in drug-resistant MM. This study identifies RPS3 as a novel biomarker and therapeutic target in MM.

2023-08-18 | GSE240978 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data