COL11A1-driven positive feedback loop modulates fibroblast transformation and activates pancreatic cancer progression.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most common leading causes of cancer death. The cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME) aggravate the malignant behavior of PDAC. However, it is still unknown how PDAC induces normal fibroblasts (NFs) to CAFs. In present research, we found that PDAC-derived collagen type XI alpha 1 (COL11A1) promoted the conversion of NFs to CAF-like cells. It included morphological and corresponding molecular marker changes. Activation of the nuclear factor-κB (NF-κB) pathway was involved in this process. Corresponding, CAFs cells could secrete interleukin 6 (IL-6), which promoted the invasion and the epithelial-mesenchymal transition of PDAC cells. Furthermore, IL-6 promoted the expression of transcription factor Activating Transcription Factor 4 by activating the Mitogen-Activated Protein Kinase/extracellular-signal-regulated kinase pathway. The latter directly promotes the expression of COL11A1. This way, a feedback loop of mutual influence was constructed between PDAC and CAFs. Our research proposed a novel concept for PDAC-educated NFs. PDAC-COL11A1-fibroblast-IL-6-PDAC axis might contribute to the cascade between PDAC and TME.

Clinical characteristics, surgical strategies, and outcome of solid pseudopapillary tumor of the pancreas: retrospective analysis in a single center.

INTRODUCTION: Solid pseudopapillary tumor of the pancreas (SPTP) is a rarely diagnosed, low-malignancy pancreatic neoplasm, which mostly can be cured by surgery. AIM: To investigate the surgical effect and prognosis of SPTP. MATERIAL AND METHODS: The data of 39 patients diagnosed with SPTP and treated with surgery between 2013 and 2020 were analyzed retrospectively. The data included the clinical characteristics, surgical management, pathological findings and therapeutic outcome. RESULTS: The mean age of the patients was 34.0 ±12.1 years, and the female : male ratio was 32 : 7. Most of the patients were asymptomatic (48.7%). The mean diameter of the tumors was 4.81 ±2.36 cm. Operative procedures were conducted according to the location and size of the tumors. Laparoscopic surgery, especially laparoscopic distal pancreatectomy (LDP), provided a smaller incision, a shorter postoperative hospital stay and a shorter postoperative fasting time. There was no observed difference in the amount of blood loss or complication rate. The median follow-up was 24 months. One patient with 20% expression of Ki-67 developed liver metastasis after surgery. CONCLUSIONS: SPTP is a rare disease with low malignancy. Minimally invasive surgery, especially LDP, has been proven to be a feasible and safe treatment method for SPTP with early recovery. The prognosis of SPTP is favorable. Lifetime surveillance is necessary especially in patients with a high expression rate of Ki-67.

LncRNA DHRS4-AS1 ameliorates hepatocellular carcinoma by suppressing proliferation and promoting apoptosis via miR-522-3p/SOCS5 axis.

Recent years have seen much effect in revealing the pathological association between lncRNA and HCC. Herein, we identified lncRNA DHRS4-AS1 as a potential tumor suppressor in HCC. Firstly, it was discovered that DHRS4-AS1 was significantly down-regulated in HCC tissues compared to normal tissues based on the database TCGA. It was also detected in a lower-than-usual expression quantity in HCC tissues we collected and HCC cell lines. Kaplan-Meier survival analysis revealed that high expression of DHRS4-AS1 contributed to higher overall survival rate of HCC patients.DHRS4-AS1 expression was significantly correlated to tumor size (P = 0.02) and TNM stage (P = 0.045). CCK-8, BrdU and colony-forming assays collectively demonstrated that overexpression of DHRS4-AS1 significantly restrained HCC cell proliferation. In vivo xenograft animal experiment showed that DHRS4-AS1 could efficiently preclude the tumor growth of HCC. Further investigation performed using flow cytometry and western blot showed that DHRS4-AS1 exerted its effects by accelerating cell apoptosis and capturing cell cycle in G0/G1 phase. Our study subsequently lucubrated that miR-522-3p was a negative target of DHRS4-AS1. Increased expression level of miR-522-3p was examined in HCC tissues and cell lines. Similarly, miR-522-3p mimics could reverse the inhibitory effect on HCC brought by DHRS4-AS1. SOCS5 was then discovered as a down-stream target of miR-522-3p, which suggested that SOCS5 participated in DHRS4-AS1/miR-522-3p axis to collectively mediate the development of HCC. Our study provides lncRNA DHRS4-AS1/miR-522-3p/SOCS5 axis as a novel target for HCC therapeutic strategy with potentiality.

Long non-coding RNA HCP5 functions as a sponge of miR-29b-3p and promotes cell growth and metastasis in hepatocellular carcinoma through upregulating DNMT3A.

Multiple studies have revealed that long non-coding RNA (lncRNAs) served as regulatory factors in modulating tumorigenesis of hepatocellular carcinoma (HCC). In the present study, we demonstrated that lncRNA HCP5 was overexpressed in HCC tissues and cell lines, and these findings were obvious even in metastatic and recurrent cases. Knockdown of HCP5 significantly alleviated cell growth, metastasis, and invasion both in vitro and in vivo through promoting apoptosis and by inactivating the epithelial-mesenchymal transition (EMT) progress. Moreover, miR-29b-3p has been identified as a negatively regulatory target gene of HCP5, and served as a tumor suppressor of HCC to prevent cell proliferation, migration, and invasion. Subsequently, DNMT3A was identified as a downstream regulatory factor of miR-29b-3p, and acted as a participated element of HCC progression by activating AKT phosphorylation. Taken together, our study elucidated for the first time that HCP5 plays a crucial role in HCC via the HCP5/miR-29b-3p/DNMT3A/AKT axis and our findings demonstrated a novel diagnostic and therapeutic strategy with potentiality to treat HCC.

Perforation caused by gastric mucosa associated lymphoid tissue lymphoma: A case report and literature review.

RATIONALE: Gastric mucosa-associated lymphoid tissue (MALT) lymphoma is the most common and best-studied extranodal marginal zone lymphoma of the MALT. It is characterized by an indolent clinical course and excellent survival compared with other malignant tumor. Complications such as obstruction, perforation or bleeding are rarely observed. The treatment strategy is still controversial. PATIENT CONCERNS: A 59-year-old man, who had been diagnosed with MALT lymphoma by gastroscopy and biopsy one month before, came to the hospital for a sudden onset of abdominal pain after breakfast. DIAGNOSES: MALT lymphoma; gastric perforation. INTERVENTIONS: Emergency surgery. OUTCOMES: Gastric perforation repair and jejunostomy was performed. The patient recovered well and is preparing for combined chemotherapy. LESSONS: This case report illustrates the challenges in diagnosis and treatment of MALT lymphoma. We discussed the particularity of its clinical characteristics, treatment strategies and prognosis combined with literature review, and we think that early diagnosis and timely appropriate chemotherapy is of great importance.