Purpose: Infantile hemangiomas (IHs) are commonly observed benign tumors that can cause serious complications. M2-polarized macrophages in IHs promote disease progression. In this study, we investigated the role of M2 macrophage-derived exosomal lncRNA MIR4435-2HG in IHs. Patients and Methods: Exosomes derived from M2 polarized macrophages were extracted. Next, using cell co-culture or transfection, we investigated whether M2 polarized macrophage-derived exosomes (M2-exos) can transport MIR4435-2HG to regulate the proliferation, migration, invasion, and angiogenesis of hemangioma-derived endothelial cells (HemECs). RNA-seq and RNA pull-down assays were performed to identify targets and regulatory pathways of MIR4435-2HG. We explored the possible mechanisms through which MIR4435-2HG regulates the biological function of HemECs. Results: M2-exos significantly enhanced the proliferation, migration, invasion, and angiogenesis of HemECs. Thus, HemECs uptake M2-exos and promote biological functions through the inclusion of MIR4435-2HG. RNA-seq and RNA pull-down experiments confirmed that MIR4435-2HG regulates of HNRNPA1 expression and directly binds to HNRNPA1, consequently affecting the NF-κB signal pathway. Conclusion: MIR4435-2HG of M2-exos promotes the progression of IHs and enhances the proliferation, migration, invasion, and angiogenesis of HemECs by directly binding to HNRNPA1. This study not only reveals the mechanism of interaction between M2 macrophages and HemECs, but also provides a promising therapeutic target for IHs.

Background: Lipofibromatosis is a rare, benign, soft tissue tumor that usually presents in children. Low incidence and lack of specificity in clinical presentation make its diagnosis difficult. Case presentation: This is a case report of a patient with a giant lipofibromatosis on the back that resembles an infantile hemangioma, which posed great difficulty in diagnosis due to atypical clinical manifestations. After the postoperative pathological and immunohistochemical examination and fluorescence in situ hybridization, the patient was finally diagnosed with lipofibromatosis. Conclusions: The incidence of fibromatosis was low. This case presents an atypical clinical manifestation since the tumor growth was on the back, and this can easily cause misdiagnosis. This case suggests that the diagnosis of lipofibromatosis depends on the pathology and fluorescence in situ hybridization.

Circular RNAs (circRNAs) are noncoding RNAs that have important roles in tumor progression. Previous studies have examined the circRNAs involved in infantile hemangioma (IH) tumors. The present study compared the circRNA levels in plasma samples from patients with IH and control individuals. The circRNA expression profiles were determined using microarray in three pairs of plasma samples from patients with proliferative IH and healthy control subjects. Expression of the identified differentially expressed circRNAs was verified using reverse transcription‑quantitative PCR (RT‑qPCR) and a bioinformatics analysis was performed to predict the microRNAs targeted by the validated circRNAs. From the circRNA expression profiles in the plasma of patients with IHs, 128 differentially expressed circRNAs were identified, of which 72 were upregulated and 56 were downregulated. The downregulated expression of three circRNAs [Homo sapiens (hsa)_circRNA_101566, hsa_circRNA_103546 and hsa_circRNA_103573] was verified using RT‑qPCR. Gene Ontology term and Kyoto Encyclopedia of Genes and Genomes pathway analyses indicated that all identified networks participated in angiogenesis and tumor formation and progression. It was determined that hsa_circRNA_101566, which is able to regulate the mTOR signaling pathway, may be an important regulatory molecule in IH development and that targeting of hsa_miR_520c is able to indirectly regulate the vascular endothelial growth factor signaling pathway. Further studies are required to clarify these effects and the underlying mechanisms.

Purpose: To investigate the role of myosin 1b (Myo1b) in infantile hemangiomas (IHs). Patients and Methods: The expression of Myo1b in IHs and normal skin tissues was evaluated using immunohistochemical techniques. Expression of Myo1b in hemangioma endothelial cells (HemECs) was detected using quantitative real-time polymerase chain reaction and Western blotting techniques. The effects of Myo1b on cell proliferation, invasion, tube formation and other biological characteristics were analyzed. A mouse model was established to observe the inhibitory effects of Myo1b in vivo. Protein expression of peroxisome proliferator-activated receptor-gamma (PPARγ) and glucose transporter 1 protein (Glut-1) in a Myo1b knockdown HemECs was detected using Western blot. Results: Myo1b was highly expressed in the proliferative stage of IHs, and promoted proliferation, invasion, and angiogenesis in vitro. Mouse models further demonstrated that Myo1b inhibited proliferation and angiogenesis of IHs. Knockdown of Myo1b inhibited Glut-1 activity, promoted expression of PPARγ transcription factor. Conclusion: Myo1b has a pro-tumor effect on IHs, knockdown of Myo1b facilitated progression of the proliferating to involution phase of IHs. Therefore, Myo1b is expected to serve as a new target for the treatment of IHs.

Ascher syndrome is a rare disorder classically characterized by blepharochalasis, double lip, and non-toxic thyroid goiter. We report a case initially diagnosed as eczema in the dermatology department, who presented with acquired double lips and blepharochalasis of the upper eyelids, without thyroid enlargement. Magnetic resonance imaging revealed uniformly increased T2-weighted signals in both the upper and lower lips, leading to a diagnosis of incomplete Ascher’s syndrome. The patient underwent oculoplastic surgery, which successfully restored the natural aesthetic contour, demonstrating the efficacy and necessity of surgical intervention. We summarize the differential diagnosis of conditions related to Ascher’s syndrome and analyze histopathological changes in the excised eyelid tissue to elucidate microscopic alterations associated with the disease.