Case report and literature review: Giant retroperitoneal cystic lymphangioma

BackgroundCystic lymphangioma is a rare benign tumor of the lymphatic system, which is most commonly observed in the neck, head and armpit.Less than 5% of lymphangiomas occur in the abdominal cavity and even less in the retroperitoneum.Case descriptionA 65-year-old male patient was diagnosed with an “abdominal mass that had persisted for 1 year, accompanied by abdominal pain, abdominal distension and dyspnea for 7 days”. After abdominal computerd tomography, a giant multilobed abdominal lymphangioma was suspected, which squeezed the intestinal canal and was closely related to the inferior vena cava. The patient underwent an exploratory laparotomy, during which, it was found that the tumor formed extensive adhesions to the transverse colon, small intestine and pelvic wall, and enveloped the abdominal aorta, superior mesenteric artery, inferior mesenteric artery and inferior vena cava to varying degrees. It was diffcult to remove the cyst completely. Postoperative pathology confirmed the diagnosis of retroperitoneal cystic lymphangioma. The patient recovered well after the operation, was eating normally by 5 days postoperatively,and was discharged 10 days postoperatively.The patient was followed up 1 month after postoperatively and no evidence of recurrence was observed.ConclusionIn this case, we report a patient with giant retroperitoneal cystic lymphangioma who underwent exploratory laparotomy combined with preoperative abdominal computerd tomography and acute abdominal pain, abdominal distension and dyspnea. Because of the large volume of the tumor and its close relationship with the superior mesenteric artery and other blood vessels, the surgeon used scissors to separate the tumor sharply and removed the whole tumor completely

ELL Protein-associated Factor 2 (EAF2) Inhibits Transforming Growth Factor beta Signaling through a Direct Interaction with Smad3

A series of in vitro and in vivo studies has shown that EAF2 can affect multiple signaling pathways involved in cellular processes. However, the molecular mechanisms underlying its effects have remained elusive. Here we report the discovery of a new functional link between EAF2 and TGF-beta signaling. Promoter reporter assays indicated that EAF2 suppresses Smad3 transcriptional activity, resulting in inhibition of TGF-beta signaling. Coimmunoprecipitation assays showed that EAF2 specifically interacts with Smad3 in vitro and in vivo but not with other Smad proteins. In addition, we observed that EAF2 binding does not alter Smad3 phosphorylation but causes Smad3 cytoplasmic retention, competes with Smad4 for binding to Smad3, and prevents p300-Smad3 complex formation. Furthermore, we demonstrated that EAF2 suppresses both TGF-beta -induced G(1) cell cycle arrest and TGF-beta -induced cell migration. This study identifies and characterizes a novel repressor of TGF-beta signaling

PELP1 Suppression Inhibits Colorectal Cancer through c-Src Downregulation

Proline-, glutamic acid-, and leucine-rich protein 1 (PELP1), a coregulator of estrogen receptors alpha and beta, is a potential protooncogene implicated in several human cancers, including sexual hormone-responsive or sexual hormone-nonresponsive cancers. However, the functions of PELP1 in colorectal cancer remain unclear. In this study, western blot and bioinformatics revealed that PELP1 expression was higher in several colorectal cancer cell lines than in immortalized normal colorectal epithelium. PELP1 silencing by short hairpin RNA promoted the senescence and inhibited the proliferation, colony formation, migration, invasion, and xenograft tumor formation of the CRC cell line HT-29. Moreover, PELP1 silencing was accompanied by c-Src downregulation. c-Src upregulation partly alleviated the damage in HT-29 malignant behavior induced by PELP1 RNA interference. In conclusion, PELP1 exhibits an oncogenic function in colorectal cancer through c-Src upregulation

Parkin promotes proteasomal degradation of p62: implication of selective vulnerability of neuronal cells in the pathogenesis of Parkinson's disease

Mutations or inactivation of parkin, an E3 ubiquitin ligase, are associated with familial form or sporadic Parkinson's disease (PD), respectively, which manifested with the selective vulnerability of neuronal cells in substantia nigra (SN) and striatum (STR) regions. However, the underlying molecular mechanism linking parkin with the etiology of PD remains elusive. Here we report that p62, a critical regulator for protein quality control, inclusion body formation, selective autophagy and diverse signaling pathways, is a new substrate of parkin. P62 levels were increased in the SN and STR regions, but not in other brain regions in parkin knockout mice. Parkin directly interacts with and ubiquitinates p62 at the K13 to promote proteasomal degradation of p62 even in the absence of ATG5. Pathogenic mutations, knockdown of parkin or mutation of p62 at K13 prevented the degradation of p62. We further showed that parkin deficiency mice have pronounced loss of tyrosine hydroxylase positive neurons and have worse performance in motor test when treated with 6-hydroxydopamine hydrochloride in aged mice. These results suggest that, in addition to their critical role in regulating autophagy, p62 are subjected to parkin mediated proteasomal degradation and implicate that the dysregulation of parkin/p62 axis may involve in the selective vulnerability of neuronal cells during the onset of PD pathogenesis