Single-cell sequencing in diffuse large B-cell lymphoma: C1qC is a potential tumor-promoting factor.

BACKGROUND: Complement component 1q (C1q) is central to the classical complement pathway. High C1q expression has been linked to poor prognosis in patients with cancer. However, the precise mechanism via which C1q contributes to diffuse large B-cell lymphoma (DLBCL) is still unknown. We aimed to explore the potential mechanism by which C1qC promoting DLBCL. METHODS: Using multiplex immunohistochemistry (mIHC) to identify immunocyte subgroups associated with prognosis in DLBCL tissues. Constructing a risk prediction model based on immunocytes using least absolute shrinkage and selection operator (LASSO) regression. Single-cell sequencing detects the expression level of C1qC in immunocytes in the DLBCL microenvironment. Using Wb and qPCR to detect markers of M2 macrophages after knocking down C1qC, and exploring the interactions between lymphoma cells and macrophages through co-culture. Analyzing clinical data from DLBCL patients to investigate the clinical significance of C1qC+ M2 macrophages. Lastly, using bioinformatics in conjunction with mIHC to elucidate the potential pro-tumor mechanism of C1qC. RESULTS: First, we found T cell subtypes, neutrophils, and M2 macrophages are associated with prognosis. Subsequently, the risk model identified C1qC as a differential gene relevant to DLBCL prognosis. Furthermore, single-cell sequencing suggested high C1qC expression in M2 macrophages. The expression level of CD163 is significantly lower following siC1qC. Co-culture experiments have shown that M2 macrophages can promote the proliferation of tumor cells and reduce their drug sensitivity. Furthermore, as an independent predictive indicator, high expression of C1qC+ M2 macrophages is associated with poor prognosis in patients. Finally, a positive correlation between increased C1qC expression and immune checkpoints, as well as an increase in the infiltration of regulatory T cells (Tregs) and M2 macrophages. CONCLUSIONS: C1qC offering new insights into pathogenesis and presenting a potential therapeutic target in DLBCL.

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.