Mucormycosis-induced upper gastrointestinal ulcer perforation in immunocompetent patients: a report of two cases.

BACKGROUND: Gastrointestinal mucormycosis (GIM) is a rare, opportunistic fungal infection with poor prognosis. Clinically, it is difficult to diagnose GIM owing to its nonspecific clinical symptoms and poor suspicion. The estimated incidence of GIM is inaccurate, and most cases are diagnosed accidentally during surgery or upon postmortem examination. GIM usually occurs in patients with immune deficiencies or diabetes. Here, we report two cases of immunocompetent young patients with GIM who had good prognosis after treatment. Compared to other case reports on GIM, our cases had unusual infection sites and no obvious predisposing factors, which make it important to highlight these cases. CASE PRESENTATION: The first case was that of a 16-year-old immunocompetent boy who was admitted with gastrointestinal bleeding and perforation due to a gastric ulcer. Strategies used to arrest bleeding during emergency gastroscopy were unsuccessful. An adhesive mass was then discovered through laparoscopy. The patient underwent type II gastric resection. Pathological examination of the mass revealed bacterial infection and GIM. The second case was of a 33-year-old immunocompetent woman with a recent history of a lower leg sprain. The patient subsequently became critically ill and required ventilatory support. After hemodynamic stabilization and extubation, she presented with hematemesis due to exfoliation and necrosis of the stomach wall. The patient underwent total gastrectomy plus jejunostomy. The pathology results revealed severe bacterial infection and fungal infection that was confirmed as GIM. The patient fully recovered after receiving anti-infective and antifungal treatments. CONCLUSIONS: Neither patient was immunosuppressed, and both patients presented with gastrointestinal bleeding. GIM was confirmed via pathological examination. GIM is not limited to immunocompromised patients, and its diagnosis mainly relies on pathological examination. Early diagnosis, timely surgical treatment, and early administration of systemic drug treatment are fundamental to improving its prognosis.

A Preliminary Study of miR-144 Inhibiting the Stemness of Colon Cancer Stem Cells by Targeting Krüppel-Like Factor 4.

Colon cancer is a prevalent clinical malignant tumor of the digestive system. The current study aims to explore the miR-144 expression in colorectal cancer (CRC) cell lines and CRC stem cells (CSCs) and to explore its effect on the stemness of CSCs and the targeted regulation of Krüppel-like factor 4 (KLF4). Use qRT-PCR to detect the expression level of miR-144 in CRC cells SW480, HCT116, and H129 and the healthy colon cell NCM460. The CSCs that were used were cultured in HCT116 cells. Use western blot to explore the expressions of Nanog, SOX2, and OCT4 stemness marker protein. After it was transfected with miR-144 mimics or KLF4 plasmid, use MTT to explore the cell viability of CSCs, use flow cytometry to evaluate apoptosis, and use transwell assay to evaluate the ability of invasive of CSCs. The targeting effect of miR-144 on the KLF4 gene was verified using TargetScan prediction and the double-luciferase reporter gene test. Use qRT-PCR to evaluate the role of miR-144 mimics on KLF4 mRNA expression in CSCs. The qRT-PCR results exhibited that the miR-144 expression in CRC cells was higher than that in the healthy colon cell line. The expressions of OCT4, Nanog, and SOX2 stem cell markers were up-regulated in CSCs, and the expression of miR144 increased in CSCs. The cell viability, apoptosis, and invasion of CSCs increased after miR-144 was transfected. The TargetScan prediction and double-luciferase reporter gene assay confirmed that miR-144 was targeted by KLF4, and the expression of KLF4 mRNA in the miR-144 mimics group reduced. Moreover, the overexpression of KLF4 could partially reverse the role of miR-144 mimics on CSCs. In summary, miR-144 was highly expressed in CRC cell lines and CSCs, and the overexpression of miR-144 in CSCs significantly promoted the proliferation of CSCs, inhibited its apoptosis, and promoted its invasion ability. In addition, its preliminary mechanism, possibly through negative regulation KLF4, promotes the stemness of CSCs, and miR-144 is likely to be a potential target for eliminating CSC from CRC treatment.

Overexpression of MAGT1 is associated with aggressiveness and poor prognosis of colorectal cancer.

Tumor metastasis and anticancer drug resistance are the major causes of mortality in patients with colorectal cancer (CRC). Due to the limitations of conventional biomarkers, it is urgent to identify novel and valid biomarkers to predict the progression and prognosis of CRC. Reverse transcription-quantitative polymerase chain reaction and western blotting were used to detect MAGT1 expression in CRC clinical samples or cell lines. Bioinformatics analysis was used to investigate the association between MAGT1 alteration and clinicopathological features of patients with CRC. The present study revealed that the transcription levels of magnesium transporter 1 (MAGT1) were significantly increased in CRC tissues compared with matched adjacent normal tissues. Overexpression of MAGT1 was associated with advanced tumor stage, N and M classification. In addition, for patients who underwent chemotherapy, patients in the MAGT1-low expression group exhibited a longer overall survival (OS) time than patients in the high-expression group. Patients with CRC treated with chemotherapy had a longer OS time than those treated without chemotherapy in the MAGT1-low expression group but not in the MAGT1-high expression group. Furthermore, MAGT1 was a valid but not an independent prognostic factor for CRC. Therefore, the present study highlighted that MAGT1 may serve as a valid biomarker for predicting the development, progression and poor prognosis of CRC.