LINC00152 knockdown suppresses tumorigenesis in non-small cell lung cancer via sponging miR-16-5p.

Background: Non-small cell lung cancer (NSCLC) is one of the most aggressive types of cancer worldwide. It has been reported that long non-coding RNAs (lncRNAs) are involved in the pathogenesis of NSCLC. In addition, LINC00152 is known to be upregulated in NSCLC. However, the mechanism underlying the effect of LINC00152 on NSCLC tumorigenesis remains to be elucidated. Methods: In the present study, cell viability, apoptosis and invasion were investigated by CCK-8, flow cytometry and Transwell assays, respectively. Reverse transcription­quantitative polymerase chain reaction and Western blotting were performed to determine the mRNA and protein expression levels. In addition, the association between LINC00152, microRNA (miR)-16-5p and BCL2-like 2 (BCL2L2) was evaluated using a dual-luciferase assay. Results: The results demonstrated that LINC00152-knockdown significantly attenuated the viability of NSCLC cells via promoting cell apoptosis. In addition, the migration and invasion ability of NSCLC cells was also decreased following transfection of cells with LINC00152 siRNA. Furthermore, miR-16-5p inhibitor or BCLCL2-overexpression reversed LINC00152 siRNA-induced NSCLC cell growth inhibition. Conclusions: The findings of the present study demonstrated that LINC00152-silencing suppressed NSCLC tumorigenesis via regulating the miR-16-5p/BCL2L2 axis. Therefore, linc00152 has the potential as a molecular marker and may be a potential target for the treatment of non-small cell lung cancer.

BCL2L13: physiological and pathological meanings.

BCL2L13 is a BCL2-like protein. It has been discovered for two decades, now on the way to be a hotspot of research with its physiological and pathological meanings found in recent years. Start with the pro-apoptotic activity, there have been reported consecutively that BCL2L13 could also induce mitochondrial fragmentation, inhibit cell death and promote mitophagy. Similar to BNIP3, BCL2L13 cannot be indiscriminately categorized into pro- or anti-apoptotic proteins. It anchors in the mitochondrial outer membrane, and expresses in various cells and tissues. This article reviews for the first time that BCL2L13 functions in physiological processes, such as growth and development and energy metabolism, and its dysregulation participating in pathological processes, including cancer, bacterial infection, cardiovascular diseases and degenerative diseases, suggesting its important roles in these events.

Successful pregnancy and delivery in a patient with chronic myeloid leukemia: a case report and review of the literature.

INTRODUCTION: Complications associated with chronic myeloid leukemia (CML) during pregnancy are rare, and management is challenging because very limited data are available on this patient group. CASE DESCRIPTION: We herein report a successful pregnancy and delivery in a patient diagnosed with CML. The patient was treated with imatinib (400 mg/day) as a first-line therapy. However, she became pregnant while she was in complete hematological remission and had a complete cytogenetic response. Because she elected to continue the pregnancy to term, imatinib treatment was stopped after 5 months of gestation and the patient was then treated with interferon-alpha for the remainder of her pregnancy. However, the CML did not relapse. She successfully gave birth to a male infant at 39 weeks by cesarean section with no adverse sequelae or malformations. DISCUSSION AND EVALUATION: The treatment of pregnant women with CML is difficult because of few available therapeutic options and limited data regarding the potential harm to the fetus. Conception should be planned and TKI therapy discontinued in female patients during pregnancy, and individual risks need to be considered when an unplanned pregnancy occurs. CONCLUSIONS: Our experience will be useful for counseling patients inadvertently exposed to tyrosine kinase inhibitors such as imatinib during pregnancy.