RESUMO
BACKGROUND: Hepatic cysts are common benign liver tumors that are typically asymptomatic. However, larger cysts, particularly giant liver cysts, can potentially induce symptoms. If the diameter of the cyst exceeds 10 cm, it can exert pressure on adjacent organs, leading to manifestations of corresponding symptoms. Here, we report the case of a complex giant hepatic cyst that caused pseudocystitis. CASE SUMMARY: A 16-year-old girl was admitted to our hospital with frequent and urgent urination. Ultrasonography revealed no obvious uterine adnexal abnormalities but showed a hypoechoic, cystic mass (173 mm × 84 mm × 138 mm) with clear boundaries, and an unclear blood flow signal in the abdominal cavity (extending from the lower edge of the left lobe of liver to the upper edge of the bladder). Abdominal contrast-enhanced computed tomography revealed a giant cystic mass in the abdominal and pelvic cavities, possibly originating from the liver, and a small amount of free fluid in the pelvic cavity, which subsequent magnetic resonance imaging confirmed. The imaging characteristics were consistent with a benign lesion. The patient underwent laparoscopic resection of the giant liver cyst with partial liver resection. Post-surgery her symptoms urinary symptoms were relieved completely and she was discharged on the sixth postoperative day. CONCLUSION: Our patient presented with symptoms suggestive of pseudocystitis, stressing the need for considering possibilities of other etiologies and differential diagnoses.
RESUMO
BACKGROUND: Our study aimed to probe the intrinsic and concrete molecular mechanism of IGF2 mRNA-binding protein 2 (IGF2BP2) in gastric cancer (GC). METHODS: The mRNA and protein expressions were assessed using qRT-PCR and western blot, respectively. CCK-8 assay was employed to determine cell proliferation. Levels of TNFα and IL-1ß were analyzed using ELISA. Furthermore, cell apoptosis was evaluated using flow cytometry analysis. Cell migration and invasion were evaluated using Transwell assay. The experiment of tumor formation in nude mice was employed to analyze the effect of IGF2BP2 in regulating GC tumor growth and lung metastasis in vivo. Finally, the binding relationship between IGF1R and IGF2BP2 was verified using RIP and RNA pull down assays. RESULTS: IGF2BP2 was significantly elevated in both GC tissues and cells. Silencing of IGF2BP2 dramatically suppressed the inflammation, proliferation, migration and invasion, yet promoted cell apoptosis in vitro and in vivo. Furthermore, IGF2BP2, as a m6A reader, was proved to increase the expression of IGF1R by identifying m6A methylation modification sites in IGF1R mRNA, thus activating RhoA-ROCK pathway. Importantly, the anti-carcinogenic impacts of IGFBP2 silence were restrained by IGF1R overexpression, which was eliminated by the inactivation of RhoA-ROCK. CONCLUSION: We emphasized the oncogenic role of IGF2BP2 in gastric carcinogenesis and confirmed its activation is partly due to the activation of IGF1R-RhoA-ROCK signaling pathway. Our findings identified that IGF2BP2 might be a promising prognostic biomarker and provided clinical translational potential.