No abstract

Purpose The long non-coding RNA MALAT1 is a predictive marker in several solid tumors with highly conserved sequences. However, the role of non-coding RNA in development of laryngeal or hypopharyngeal cancer remains unclear. Methods Tumor tissues and adjacent non-cancer tissues of 24 patients were collected. We detected the expression of MALAT1 in laryngeal cancer tissues and hypopharyngeal cancer tissues. Moreover, we developed a MALAT1 silencing model in human laryngeal tumor cells by transfecting MALAT1 small interfering RNA into human laryngeal carcinoma cell line Hep-2 and pharyngeal carcinoma cell line FaDu with Lipofectamine 2000 system. Cell cycle analysis, Cell Counting Kit-8 assay, Transwell assay, quantitative reverse transcription PCR, and wound-healing assays were performed to evaluate the impact of MALAT1 depletion on laryngeal or hypopharyngeal cancer cell's growth, proliferation, apoptosis, invasion and migration. Results MALAT1 was significantly up-regulated in laryngeal and hypopharyngeal carcinoma cells. MALAT1 down-regulation induced the increased apoptosis of both cell lines and suppressed cells' proliferation. Cells were arrested in G1/G2 phase and cells of S phase were significantly decreased. Down-regulation of MALAT1 expression can also inhibit the migration and invasion of laryngeal squamous cell carcinoma cell (Hep-2) and hypopharyngeal cancer cell (FaDu). Conclusion In summary, our deactivation model of MALAT1 disentangled the active function of it as a regulator of gene expression governing the hallmarks of laryngeal and hypopharyngeal cancer. Blocking this long non-coding RNA may restrain the development of laryngeal cancer.

Small-cell lung cancer (SCLC) presenting with syncope as the initial symptom is rare in adults. This onset of tumour-induced syncope cannot be screened or differentiated by coronary angiography, magnetic resonance angiography of the neck or 24-hour dynamic electrocardiogram. We herein describe the case of a 61-year-old man who presented with recurrent syncope that resolved after the first course of chemotherapy (carboplatin plus etoposide) for SCLC. A mass measuring 57×53 mm was identified in the left hilum, and a diagnosis of limited-disease SCLC (T4N2M0, IIIB) was made. Considering the rapid and complete remission after the treatment of the primary lesion, we hypothesised that the syncope was neurogenic and associated with cancer. Thus, 8 similar cases retrieved from PubMed were reviewed and, for the first time, the mechanism underlying the syncope was identified, which may involve tumour location, neurobiology and other inducing factors. Thus, for the treatment of such SCLC patients, standard chemotherapy is crucial for preventing syncopal attacks.