Gli promotes tumor progression and metastasis through regulating EMT in non–small-cell lung cancer

Abstract

CTCs)) and tumour biopsy samples. Results: The median age of pts was 56 (range 32-75). 48% (33/68) were colon tumours, 34% (23/68) rectal, 9% (6/68) rectosigmoid and 7% (5/68) small bowel. Pts had failed an average of 3 lines (range 1-5) of treatment prior to recruitment. 74% (50/68) of patients had both sufficient tumour DNA in their plasma, and archival biopsies for analysis. Sequencing of ctDNA detected all mutations reported in tumour in 76% (38/ 50) of pts. ctDNA analysis picked up additional mutations in 30% (15/50) of pts. The interval between collection of archival biopsies and blood tests (p ¼ 0.300) did not affect detection of new mutations. 31% (6/19) of pts treated with anti-EGFR therapy developed recognised resistance mutations (KRAS and EGFR) in ctDNA on serial analysis. The most commonly detected mutations were TP53 (60%), KRAS (51%), PIK3CA (15%) and PTEN (3%). Other mutated genes included CTNNB1, BRAF, FGFR3 and ERRB2. Pre-clinical models (organoids and patient-derived xenografts (PDX)) were attempted from blood (CTCs) and/or tumour tissue in 29% (20/68) of pts. CTC organoid cultures were optimised and successful in 1/17 pts. Conclusions: ctDNA may be used for routine molecular characterisation of metastatic SBC/CRC and results can be analysed to track the development of resistance.

Novel long non‐coding RNA LINC02323 promotes epithelial‐mesenchymal transition and metastasis via sponging miR‐1343‐3p in lung adenocarcinoma

“…A wealth of evidence suggests that epithelial-mesenchymal transition (EMT) plays pivotal roles in migration and metastasis of tumor cells. [4][5][6] Transforming growth factor-β (TGF-β) is major inducer of EMT, which is known to be expressed in most adenocarcinomas including LUAD and associates with cancer cell metastasis. [7][8][9][10] Long noncoding RNAs (lncRNAs) are defined as transcripts of length > 200 nucleotides with a low coding potential.…”