Morsingiqbal6847

Lung adenocarcinoma (LUAD), which is the most important and common subtype of non-small cell lung cancer (NSCLC), is highly heterogeneous with a poor prognosis and poses great challenges to health worldwide. MicroRNAs (miRNAs) are regulators of gene expression with recognized roles in physiology and diseases, such as cancers, but little is known about their functional relevance to CD8

T cell infiltration regulation in the tumor microenvironment (TME) of NSCLC patients, especially LUAD patients.

Bioinformatic analysis was used to analyze TCGA data. RT-PCT, Western blot, luciferase assay and immunohistochemistry were used to detect the expression levels and bindings of genes and miRNA. ELISA and cytotoxic assay were used to evaluate CD8

T cell function.

In this study, bioinformatic analysis unveiled the miR-505-3p/NET1 pair as a CD8

T-tumor-infiltrating lymphocyte (TIL) regulator. Then, we confirmed the bioinformatic results with LUAD patient samples, and NET1 was shown to be a direct target of miR-505-3p in a luciferase assay. Functional experiments demonstrated that miR-505-3p enhanced CD8

T-TIL function, while NET1 impaired CD8

T-TIL function and partly reversed the effects of miR-505-3p. The observed effects might be exerted via the regulation of immunosuppressive receptors in T cells.

Our study may provide novel insights into LUAD progression related to the TME mechanism and new possibilities for improving adoptive immunotherapy.

Our study may provide novel insights into LUAD progression related to the TME mechanism and new possibilities for improving adoptive immunotherapy.

Long non-coding RNA is involved in the genesis and development of various tumors, and it has been found through database screening that LINC01087 is highly expressed in breast cancer (BC), but mechanisms of LINC01087 in BC are still under investigation. Therefore, this study aimed to study relevant mechanisms of LINC01087 in BC to provide potential therapeutic targets for the disease in clinic practice.

The qRT-PCR assay was applied to determine the LINC01087 expression in BC, and the cell counting kit-8 (CCK8) assay, transwell assay, and flow cytometry were used to analyze the proliferation, apoptosis, and invasion of breast cancer cells (BCCs), respectively. The Western blot assay was used to determine the ROCK1 expression, and the luciferase reporter gene assay, RNA-binding protein immunoprecipitation (RIP), and RNA pull-down assays were applied to study the interaction between LINC01087 and miR-335-5p. Moreover, tumor xenotransplantation was conducted in nude mice to explore the effects of LINC01087 oof ROCK1 and affect the invasion and migration of BCCs.

Hepatocellular carcinoma (HCC) is a common malignancy worldwide with a high mortality rate. lncRNA

is highly expressed in HCC. We aimed to study the role of

in HCC and its relationship with miR-4766-5p.

The levels of

in HCC tissues and cell lines were determined. Relationship between

and clinical features and prognosis was studied. The influence of

on HCC cell viability, migration, invasion and apoptosis was studied in vitro. Rescue experiments were conducted after the binding site between

and miR-4766-5p confirmed by dual-luciferase assay. The protein expression of AKT, p-AKT, mTOR and p-mTOR in HCC cells with knockdown of

was determined by Western blotting. A tumor study in nude mice was conducted in order to assess the effects of

on tumor growth characteristics.

was up-regulated in HCC tissues and cell lines.

expression was closely related to tumor size, vascular invasion and TNM stage. Knockdown of

inhibited HCC cell viability, migration and invasion and promoted cell apoptosis. MiR-4766-5p was a target of

and knockdown of

could decrease the protein expression of p-AKT and p-mTOR. Rescue experiments showed that miR-4766-5p mimics could attenuate the promoting role of

on HCC cell viability, invasion and migration, and inhibiting role on cell apoptosis. Moreover, we used nude mice models and also found that the knockdown of

reduced tumor volume and weight.

lncRNA

could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC.

lncRNA SFTA1P could promote tumor development in HCC by down-regulating miR-4766-5p expression via PI3K/AKT/mTOR signaling pathway. It may be a potential therapeutic target for HCC.

Most epidermal growth factor receptor (EGFR) exon 20 insertion (ex20ins) mutations are resistant to tyrosine kinase inhibitors (TKIs). While some non-small cell lung cancer (NSCLC) patients harboring special subtypes of

ex20ins still achieved clinical response after TKIs treatment, identifying special subtypes of

ex20ins is helpful to find out NSCLC patients who can respond to TKIs.

A 71-year-old non-smoker Chinese female was diagnosed with advanced lung adenocarcinoma harboring

ex20ins (N771delinsKG). The patient received first-line afatinib (40 mg/day) therapy and a significant and substantial reduction in tumor size was observed subsequently. According to RESIST 1.1, a radiological partial response was achieved. The final progression-free survival was 10 months.

This is the first published case report of

N771delinsKG lung adenocarcinoma, which highlighted the heterogeneity of clinical response to TKIs for

ex20ins-mutant NSCLC. Such results need to be further investigated in prospective studies.

This is the first published case report of EGFR N771delinsKG lung adenocarcinoma, which highlighted the heterogeneity of clinical response to TKIs for EGFR ex20ins-mutant NSCLC. Such results need to be further investigated in prospective studies.

Long non-coding RNAs (lncRNAs), which are key regulators of gene expression, are involved in lung cancer progression. Although numerous differentially expressed lncRNAs have been reported, merely a limited number of studies have been performed to verify their functions in lung cancer.

RNA sequencing data were re-analyzed to investigate the GATA6-AS1 expression in lung cancer. RT-qPCR was performed to verify the expression of GATA6-AS1 in collected tissue samples and cell lines. CCK-8 and transwell assays were carried out to evaluate the role of GATA6-AS1 in lung cancer cells. Dual-luciferase reporter assay and bioinformatic analysis were used to explore the miRNA which can be sponged by GATA6-AS1 in lung cancer cells.

Currently, we focused on exploring the role and mechanisms of GATA6-AS1 in lung cancer. VER155008 cost Expression of GATA6-AS1 was decreased in lung cancer based on the analysis of RNA sequencing dataset, TCGA data and RT-qPCR of clinical tissue samples. Via overexpression of GATA6-AS1, it was revealed that GATA6-AS1 inhibited lung cancer cell proliferation and invasion.