Expression of -mutant proteins and genomic evolution in -mutant transformed small cell lung cancer.

Background: The transformation of epidermal growth factor receptor ()-mutant lung adenocarcinoma (LUAD) into small cell lung cancer (SCLC) accounts for 3-14% of the resistance mechanism to EGFR tyrosine kinase inhibitors (TKIs). At present, there is no relevant research to explore the dynamic expression of -mutant proteins and genomic evolution in -mutant transformed SCLC/neuroendocrine carcinoma (NEC).

Methods: Genetic analysis and protein level analysis by next-generation sequencing (NGS), Whole-exome sequencing (WES) and immunohistochemistry were performed to explore expression of -mutant proteins and genomic evolution in -mutant transformed SCLC.

Pathological characteristics and tumour immune microenvironment of lung malignancies with RET rearrangement.

Background: For patients with lung malignancies with RET rearrangement, the efficacy of immune checkpoint inhibitors is limited. The characteristics of the tumour immune microenvironment (TIME) and molecular pathological features of these patients have not been well elucidated. We aimed to investigate their clinical outcomes and explore characteristics of TIME, using multiplex immunohistochemistry technology (mIHC).

[Advances in the Treatment of RET Fusion-positive Advanced Non-small Cell Lung Cancer].

Rearranged during transfection (RET) fusions are found in 0.7% to 2% of non-small cell lung cancer (NSCLC). Fusions between RET gene and other domains represent the distinct biological and clinicopathological subtypes of NSCLC.

Downregulation of HOXA1 gene affects small cell lung cancer cell survival and chemoresistance under the regulation of miR-100.

Chemoresistance is often developed in small cell lung cancer (SCLC) patients and leads to poor prognosis. Hox genes, a highly conserved family, play a crucial role in apoptosis, receptor signalling and differentiation. MicroRNAs (miRNAs) have also been shown to play a crucial role in these biological processes by regulating the target genes.

[Role of homeobox gene A5 in multidrug resistance of human small cell lung cancer cells].

Objective: To investigate the role of homeobox gene A5 (HOXA5) in multidrug resistance of human small cell lung cancer (SCLC) cells and the possibility of using HOXA5 as the therapeutic targets for SCLC treatment.

Methods: We examined HOXA5 mRNA and protein expressions in chemosensitive human SCLC cells (H69) and the multidrug-resistant SCLC cells (H69AR) using quantitative real-time PCR and immunoblotting. HOXA5 expression was then enhanced or suppressed by transfection of the cells with HOXA5 expression plasmids or small interference RNA (siRNA), and the chemosensitivity of transfected cells to cisplatin (DDP) and etoposide (VP-16) was evaluated using cell counting kit-8 (CCK8) assay.

MiR-296-3p regulates cell growth and multi-drug resistance of human glioblastoma by targeting ether-à-go-go (EAG1).

MicroRNAs (miRNAs) - short non-coding RNA molecules - post-transcriptionally regulate gene expressions and play crucial roles in diverse biological processes such as development, differentiation, apoptosis and proliferation. In order to investigate the possible role of miRNAs in the development of multi-drug resistance (MDR) in human glioblastoma, we first detected (by Western blotting, real-time polymerase chain reaction [RT-PCR] and immunohistochemistry) the expression of miR-296-3p and ether-à-go-go (EAG1 or KCNH1) in U251 cells, U251/imatinib mesylate (U251AR cells) and clinical specimens. The results showed that miR-296-3p was down-regulated in U251AR cells, concurrent with the up-regulation of EAG1 protein, compared with the parental U251 cell line.

Gene expression profiling of drug-resistant small cell lung cancer cells by combining microRNA and cDNA expression analysis.

MicroRNAs (miRNAs) are now known to play important roles in the regulation of gene expression for developmental timing, cell proliferation and apoptosis. Therefore, it is likely that they also modulate sensitivity and resistance to anti-cancer drugs. To better understand the molecular mechanisms of multidrug resistance in SCLC and identify novel molecular markers, we evaluated the expression of 856 miRNAs and approximately 22,000 genes using miRNA microarray and cDNA microarray in cellular models of SCLC which were widely used as sensitive (NCI-H69) and resistant cell lines (NCI-H69AR) to chemotherapy.

Depletion of PI3K p85alpha induces cell cycle arrest and apoptosis in colorectal cancer cells.

Colorectal cancer is one of the most common malignancies in the world. Overactivity of phosphatidylinositol 3-kinase (PI3K) is frequently detected in colorectal carcinoma. PI3K signaling plays a pivotal role in intracellular signal transduction pathways involved in cell growth, cellular transformation, and tumorigenesis.

[PI3K p85alpha expression and its role in the progression of colorectal cancer].

Objective: To investigate the expression of PI3K p85alpha in normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma and explore its significance in the progression of colorectal cancer.

Methods: The expression of PI3K p85alpha was detected in 116 normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma specimens using immunohistochemical staining, and the relationship between the expression of PI3K p85alpha protein and the clinicopathological factors was analyzed.

Results: The positivity rates of the expression of PI3K p85alpha protein increased gradually in the progression of colorectal cancer and showed significant differences between the tissues (P<0.