PRDX2 regulates stemness contributing to cisplatin resistance and metastasis in bladder cancer.

BACKGROUND: Cisplatin (CDDP)-based chemotherapy has emerged as the primary treatment for muscle-invasive bladder cancer and metastatic bladder cancer. Nevertheless, a significant proportion of patients experience rapidly developed chemoresistance, leading to treatment ineffectiveness. Existing evidence suggests that chemoresistance is governed by various factors, including tumor stem cells, epithelial mesenchymal transition, and reactive oxygen species (ROS). However, limited research has been conducted on the role of PRDX2, a crucial ROS scavenger, in the modulation of chemoresistance in bladder cancer. METHODS: Cisplatin-resistant cell lines were established using the concentration gradient overlay method, and differentially expressed genes in resistant cells were screened through RNA sequencing. The expression of PRDX2 in cells and tissues was assessed using RT-qPCR, Western Blot, and immunohistochemistry. The expression of PRDX2 in bladder cancer and adjacent tissues was evaluated using a bladder cancer tissue microarray. Furthermore, the impact of PRDX2 knockdown on tumor formation and metastasis was investigated in vivo by applying subcutaneous tumor xenografts tail vein metastasis assays. RESULTS: We demonstrated that PRDX2 is significantly upregulated in bladder tumors and cisplatin-resistant bladder tumor cell lines. Overexpression of PRDX2 can promote tumor proliferation, migration, and invasion both in vitro and in vivo. We have found that knockdown of PRDX2 expression can effectively reverse cell resistance to cisplatin. Mechanistically, our findings suggest that PRDX2 is involved in regulating tumor stemness and epithelial-mesenchymal transition (EMT). Knockdown of PRDX2 affects the PI3K-AKT and mTOR signaling pathways, thereby influencing tumor stemness and EMT, ultimately impacting the chemotherapy resistance of the tumor. CONCLUSIONS: This study provides a new insight into the regulation of chemotherapy resistance in bladder cancer by PRDX2. Targeting PRDX2 can serve as a potent therapeutic target for chemotherapy resistance.

Risk factors for intraoperative blood loss in resection of intracranial meningioma: Analysis of 530 cases.

PURPOSE: Excision of intracranial meningioma has been associated with major intraoperative blood loss (IBL). The objective of the study was to identify factors affecting IBL during removal of meningioma. METHODS: We retrospectively studied medical records of 530 adult patients who underwent surgery for intracranial meningioma at Sichuan Provincial People's Hospital between September 2018 and May 2022. We obtained the following data from each patient's medical chart: age, sex, height, weight, comorbidities, blood pressure, history of smoking and alcohol, imaging examination findings, pathologic diagnosis, albumin, creatinine, calcium, magnesium, hemoglobin (Hb), hematocrit, platelet count, activated partial thromboplastin time, international normalized ratio, fibrinogen concentration and blood transfusion. Univariate and multivariate analyses were performed to identify risk factors for greater IBL during removal of intracranial meningioma. RESULTS: A total of 530 patients were included in our study. Univariate analysis revealed that sex (p = 0.004), two-dimensional (2D) tumor area (p < 0.001), sinus involvement (p = 0.014), World Health Organization grade (p = 0.015), preoperative albumin level (p = 0.032), preoperative Hb level (p = 0.001) and preoperative platelet count (p = 0.004) were significantly associated with greater IBL. Multivariate analysis revealed that greater 2D tumor area (p < 0.001), higher preoperative albumin concentration (p = 0.029) and higher preoperative platelet count (p = 0.03) were independent risk factors for greater IBL in resection of intracranial meningioma. CONCLUSION: Larger tumor size, higher preoperative albumin concentration and higher preoperative platelet count were identified as independent risk factors for greater IBL in resection of intracranial meningioma.

The effects of Malassezia in the activation of Interleukin (IL)-23/IL-17 axis in Psoriasis.

We explore the association of Malassezia and IL-23/IL-17 axis in the skin lesions of patients with Psoriasis. From October 2018 to October 2020, 202 psoriasis patients were hospitalized in the dermatology department of Yantaishan hospital. The patients' skin lesions were collected, and Malassezia-specific mRNA in the skin lesions was determined. The patients were subdivided into Malassezia high and low distribution groups as per the Malassezia-specific mRNA results. Psoriasis Area and Severity Index (PASI) scores between the two groups were performed. LL-37, IL-23, IL-17A, and tumor necrosis factor α (TNF-α) expression in the skin lesions of the two groups were determined. Malassezia mRNA and the correlation of LL-37 with inflammatory factors TNF-α, IL-23, and IL-17A were determined. The relevance of inflammatory factors, Malassezia infection, and LL-37 content with PASI score were studied. The Malassezia high distribution group was treated with etoconazole, and the effects of treatment on the PASI score, IL-23, TNF-α, and IL-17A were determined. The PASI score, neutrophil, eosinophil, and peripheral blood white blood cell counts, and lgG in the Malassezia high distribution group were significantly higher than in the low distribution group (P<0.05). IL-23, LL-37, TNF-α, and IL-17A levels in the Malassezia high distribution group were significantly higher than in the low distribution group (P<0.05). Malassezia and LL-37 levels had a moderate positive correlation (R=0.5009, P<0.0001). Malassezia and LL-37, IL-17A, TNF-a, and IL- 23 correlated positively. Malassezia, IL-17A, LL37, TNF-a, and IL-23 correlated positively with the PASI score of Psoriasis. Ketoconazole therapy inhibited the PASI score, IL-23, TNF-a, and IL-17A expressions in patients. Malassezia enhances the progression of Psoriasis through the aberrant activation of the IL-23/IL-17 axis.

MicroRNA miR-124-3p suppresses proliferation and epithelial-mesenchymal transition of hepatocellular carcinoma via ARRDC1 (arrestin domain containing 1).

Hepatocellular carcinoma (HCC) is responsible for high morbidity and mortality worldwide. Increasing evidence suggests that microRNAs intensively participate in HCC development and progression. In the current study, we aimed to explore the impact of miR-124-3p in the proliferation and epithelial-mesenchymal transition (EMT) of HCC. The RT-qPCR assay was employed to determine miR-124-3p expression in human HCC specimens and cell lines. Luciferase assay was used to validate the miR-124-3p target gene. Western Blot and RT-qPCR were performed to study the effects of miR-124-3p modulation on ARRDC1 (Arrestin Domain Containing 1) mRNA and protein expressions. MTT assay, wound healing assay, EdU assay, and Transwell assay were utilized to verify the impact of miR-144-3p modulation on HCC proliferation and EMT via ARRDC1. We found that MiR-124-3p expression downregulates in HCC. Overexpression of miR-124-3p reduced the HCC cell proliferation and EMT. Meanwhile, we determined that the expression of ARRDC1 is increased in HCC, and miR-124-3p directly binds the 3'UTR of ARRDC1 and inhibits its expression at mRNA and protein level, suggesting that miR-124-3p was capable of negatively modulating ARRDC1. Besides, cotransfection of ARRDC1-overexpression plasmid and miR-124-3p mimics increased the cell proliferation and EMT as compared to miR-124-3p mimics. Our study concluded that miR-124-3p directly binds the 3'UTR of ARRDC1 and exerts anti-tumorous effects by inhibiting the HCC proliferation and EMT. Therefore, miR-124-3p/ARRDC1 axis may serve as a novel therapeutic target to inhibit HCC growth and metastasis.

miR-455 Inhibits the Viability and Invasion by Targeting RAB18 in Hepatocellular Carcinoma.

BACKGROUND: Hepatocellular carcinoma (HCC) has been regarded as the fifth most common cancer worldwide with a low prognosis. miR-455 usually played the role of a tumor suppressor in multiple cancers. The aim of this study was to investigate the roles of miR-455 in HCC. MATERIALS AND METHODS: Cell viability and invasion were measured by CCK8 and Transwell assays. Luciferase reporter assay was performed to verify that miR-455 directly binds to the 3'-noncoding region (UTR) of RAB18 mRNA in Huh7 cells. RESULTS: The expression of miR-455 was lower in HCC tissues and cell lines than in nontumor tissues and normal cell line, and downregulation of miR-455 was connected with worse outcome of HCC patients. miR-455 suppressed cell proliferation in vitro and in vivo, and it inhibited the abilities of cell invasion and EMT in HCC. RAB18 was upregulated in HCC tissues and cell lines, and the expression of RAB18 was regulated by miR-455. RAB18 reversed partial roles of miR-455 on cell viability and invasion in HCC. CONCLUSION: miR-455 inhibited cell viability and invasion by directly targeting the 3'-UTR of RAB18 mRNA of hepatocellular carcinoma.

Pineal Region Glioblastomas: Clinical Characteristics, Treatment, and Survival Outcome.

OBJECTIVE: Given the rarity of patients with pineal glioblastoma (GBM), clinical characteristics, treatment, and prognostic factors are not well characterized. This study aimed to investigate these characteristics and identify the prognostic factors of overall survival (OS). METHODS: A retrospective analysis of newly diagnosed patients with pineal GBM, including our 3 cases and an additional 44 cases from published articles, was conducted. Survival analysis was performed by Kaplan-Meier analysis and Cox regression analysis was used to determine the prognostic factors. RESULTS: A total of 47 patients (28 males and 19 females) were enrolled, with a median age of 46 years (range, 5-74 years). Forty-four patients (90.9%) had preoperative obstructive hydrocephalus. Among 38 patients, 21 (55.3%) had distal leptomeningeal dissemination. Forty-five patients (95.7%) had resection/biopsy, 6 of whom had gross total resection, 22 had subtotal resection, 7 had partial resection, and 10 had biopsy. Adjuvant therapy included radiotherapy in 36 patients and chemotherapy in 27 patients. The median OS was 10.0 months. The 6-month, 1-year, and 2-year survival was 68.0%, 42.6%, and 17.0%, respectively. Cox regression analysis showed that patients receiving biopsy (P = 0.042) or chemotherapy (P = 0.029) had the better OS and these were regarded as independent prognostic factors. Further survival analysis showed that chemoradiotherapy had better survival benefit than other regimens. CONCLUSIONS: In this study, we summarized the characteristics of patients with pineal GBM and showed the correlation between clinical characteristics and prognosis. This study may give readers a deep understanding of these rare GBMs and provide some references for future management.

Risk factors for hydrocephalus following fourth ventricle tumor surgery: A retrospective analysis of 121 patients.

BACKGROUND AND AIM: Most patients who present with a fourth ventricle tumor have concurrent hydrocephalus, and some demonstrate persistent hydrocephalus after tumor resection. There is still no consensus on the management of hydrocephalus in patients with fourth ventricle tumor after surgery. The purpose of this study was to identify the factors that predispose to postoperative hydrocephalus and the need for a postoperative cerebrospinal fluid (CSF) diversion procedure. MATERIALS AND METHODS: We performed a retrospective analysis of patients who underwent surgery of the fourth ventricle tumor between January 2013 and December 2018 at the Department of Neurosurgery in West China Hospital of Sichuan University. The characteristics of patients and the tumor location, tumor size, tumor histology, and preventive external ventricular drainage (EVD) that were potentially correlated with CSF circulation were evaluated in univariate and multivariate analysis. RESULTS: A total of 121 patients were enrolled in our study; 16 (12.9%) patients underwent postoperative CSF drainage. Univariate analysis revealed that superior extension (p = 0.004), preoperative hydrocephalus (p<0.001), and subtotal resection (p<0.001) were significantly associated with postoperative hydrocephalus. Multivariate analysis revealed that superior extension (p = 0.013; OR = 44.761; 95% CI 2.235-896.310) and subtotal resection (p = 0.005; OR = 0.087; 95% CI 0.016-0.473) were independent risk factors for postoperative hydrocephalus after resection of fourth ventricle tumor. CONCLUSION: Superior tumor extension (into the aqueduct) and failed total resection of tumor were identified as independent risk factors for postoperative hydrocephalus in patients with fourth ventricle tumor.

Long-Chain Non-Coding SOX21-AS1 Promotes Proliferation and Migration of Breast Cancer Cells Through the PI3K/AKT Signaling Pathway.

AIM: This study aimed to investigate the effect of long-chain non-coding SOX21-AS1 on the proliferation and migration of breast cancer (BC) cells through the PI3K/AKT signaling pathway. METHODS: Eighty-eight BC and adjacent tissues were collected, and BC cells and normal breast epithelial cells were purchased. LncRNA SOX21-AS1 expression in tissues and cells was detected by RT-PCR. miR-NC, si-SOX21-AS1, and Sh-SOX21-AS1 were transfected into BC cells. The PI3K/AKT signaling pathway was interfered with L740Y-P (activator of the PI3K/AKT pathway) and LY294002 (inhibitor of the PI3K/AKT pathway) in BC cells. The SOX21-AS1 expression in BC tissues and cells was tested by qRT-PCR, and the expression levels of p-PI3K, p-AKT, N-cadherin, E-cadherin, and vimentin were detected by WB. RESULTS: SOX21-AS1 was highly expressed in BC, and the p-PI3K and p-AKT levels were also high. Cell experiments showed that inhibiting SOX21-AS1 expression could inhibit the proliferation, invasion, migration, and EMT of BC cells, and up-regulating its expression could promote the proliferation, invasion, migration, and EMT of ovarian cancer cells. The tumor-forming experiment in nude mice was consistent with the results in vitro. 740Y-P intervention could reverse the inhibition effect of Si-SOX21-AS1 on BC cell proliferation, invasion, migration, and EMT, while LY294002 intervention could reverse the promotion effect of Sh-SOX21-AS1 on BC cell proliferation, invasion, migration, and EMT. CONCLUSION: SOX21-AS1 is highly expressed in BC tissues. Silencing BC expression can inhibit the proliferation, invasion, migration, and EMT of cells by inhibiting the PI3K/AKT signaling pathway, which may be a new target for diagnosis and treatment.

Clinical value of color Doppler ultrasound combined with serum CA153, CEA and TSGF detection in the diagnosis of breast cancer.

In the present retrospective study, the clinical value of color Doppler ultrasound combined with the detection of the serum tumor markers carbohydrate antigen 153 (CA153), carcinoembryonic antigen (CEA) and tumor specific growth factor (TSGF) as diagnostic tools for breast cancer was investigated. A total of 103 patients with breast cancer and 50 patients with benign breast lesions were enrolled in the study. All patients were examined by color Doppler ultrasonography. Electrochemiluminescence was used to measure the expression levels of CA153 and CEA, and chemical colorimetric assay for the measurement of TSGF expression. The differences in mass boundary, morphology, internal echo, calcification, peak blood flow velocity (Vmax), resistance index (RI), pulsatility index (PI) and blood flow signal classification between the two groups were statistically significant (P<0.05). The expression levels of CA153, CEA and TSGF in the serum of patients in the breast cancer group were significantly higher than those in the benign lesion group (P<0.01). In the breast cancer group, CA153, CEA and TSGF expression levels were significantly higher in patients with high-stage cancer and recurrence, compared with the patients with low-stage cancer and no recurrence. The sensitivity, accuracy and negative predictive value of the combined detection were significantly improved compared with those of the single tests (P<0.01). Color Doppler ultrasound combined with the detection of CA153, CEA and TSGF levels in the serum of patients can be used as an effective tool that can improve the accuracy of breast cancer diagnosis leading to early diagnosis and clinical intervention.

Risk factors for the recurrence of world health organization grade â ¡ ependymomas of spinal cord in adults after microsurgical resections: A retrospective study of 118 patients in a single center.

OBJECTIVE: To identify the risk factors for recurrence of World Health Organization (WHO) grade Ⅱ ependymomas of spinal cord in adults after microsurgical resections. PATIENTS AND METHODS: A total of 118 adult patients diagnosed with WHO grade Ⅱ ependymomas of spinal cord at west china hospital from January 2010 to December 2016 were reviewed retrospectively. To identify the risk factors for recurrence, we performed univariate analyses and multivariate logistic regression analyses successively. RESULTS: Twelve patients had a recurrence with a median recurrence time of 30 months [inter-quartile range (IQR) 23.5-75.5 months]. Univariate analysis showed that age (p = 0.030), STR (p < 0.001), index of Ki-67 (p = 0.004), and Vimentin (+, p = 0.004) were associated with postoperative recurrence of ependymomas of spinal cord in adults, while univariate analysis showed that only STR [odds ratio (OR) = 18.838, 95 % confidence interval (CI): 3.068-115.673; p = 0.002], index of Ki-67 (OR = 1.381, 95 % CI: 1.021-1.868; p = 0.036), Vimentin (+; OR = 6.706, 95 % CI: 1.218-36.928; p = 0.029) were independent risk factors for recurrence. CONCLUSIONS: The recurrence rate of WHO grade Ⅱ ependymomas of spinal cord in adults was about 13.6 %. Subtotal resection is a critical risk factor for recurrence. A high index of Ki-67 is another independent risk factor for recurrence. Positive Vimentin may also play a role in this process. GTR is very important to prevent recurrence after operation if it is safe to conduct. In cases with higher index Ki-67 and Vimentin (+), close follow-ups are necessary.

Risk factors for postoperative pneumonia in patients with posterior fossa meningioma after microsurgery.

OBJECTIVES: Postoperative pneumonia (POP) is one of the common complications associated with mortality and morbidity. Even so, it has received little intensive research after microsurgical removal for posterior fossa meningioma (PFM). In this study, we aimed to identify perioperative factors for POP after PFM microsurgery to risk-stratify patients and improve clinical outcomes. PATIENTS AND METHODS: We retrospectively review on all patients who underwent microsurgical resection (n = 321) for PFM from January 2016 to December 2018. To identify the risk factors for POP, we performed univariate and multivariate analyses successively. RESULTS: 44 (13.7%) patients were diagnosed as POP. In accordance with univariate analysis, postoperative Glasgow Coma Scale (GCS) score (<13; p < 0.001), tumor size (≥3cm; p < 0.001), procedure duration (≥3 h; p < 0.001), tumor located in anterior or lateral of brainstem (p < 0.001), estimated blood loss (EBL; > 1000ml; p = 0.001) and brainstem shift (p < 0.001) were associated with POP. By multivariate analysis, the first four were independent risk factors for POP. The study also revealed that POP brought about extended duration of postoperative hospitalization. CONCLUSION: The incidence of POP following PFM microsurgery was significantly high (13.7%). Apart from tumor size (≥3cm) and procedure duration (≥3 h), GCS score (<13) and tumor located in anterior or lateral of brainstem were independent risk factors for POP. Efforts to reduce the duration of surgery, especially among the large tumors located in anterior or lateral of brainstem, may reduce POP rate and hospitalization stay.

Sphingobacterium olei sp. nov., isolated from oil-contaminated soil.

A Gram-stain-negative, rod-shaped, non-motile and non-spore-forming bacterium, designated HAL-9T, was isolated from oil-contaminated soil in Daqing oilfield, Heilongjiang Province, PR China. Strain HAL-9T was able to degrade quizalofop-p-ethyl and diclofop-methyl. Growth was observed at 10-35 °C (optimum, 30 °C), pH 6.0-10.0 (optimum, pH 7.0) and salinity of 0 %-5.0 % (w/v; optimum 1.0 %). The results of phylogenetic analysis based on the 16S rRNA gene indicated that strain HAL-9T belongs to the genus Sphingobacterium and showed the highest sequence similarity (98.3 %) to Sphingobacterium alkalisoli Y3L14T, followed by Sphingobacterium mizutaii DSM 11724T (95.1 %) and Sphingobacterium lactis DSM 22361T (95.1 %). Menaquinone-7 (MK-7) was the only isoprenoid quinone. The predominant cellular fatty acids were summed feature 3 (C16 : 1 ω7c and/or C16 : 1 ω6c), iso-C15: 0 and iso-C17 : 0 3-OH. The major polar lipids were phosphatidylethanolamine, three phosphoglycolipids and three unidentified lipids. The draft genome of strain HAL-9T was 5.41 Mb. The G+C content of strain HAL-9T was 40.6 mol%. Furthermore, the average nucleotide identity and in silico DNA-DNA hybridization values between strain HAL-9T and S. alkalisoli Y3L14T were 86.2 % and 32.8 %, respectively, which were below the standard thresholds for species differentiation. On the basis of phenotypic, genotypic and phylogenetic evidence, strain HAL-9T represents a novel species in the genus Sphingobacterium, for which the name Sphingobacterium olei sp. nov. is proposed. The type strain is HAL-9T (=ACCC 61581T=CCTCC AB 2019176T=KCTC 72287T).

lncRNA CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop drives progression of acute myeloid leukaemia.

Acute myeloid leukaemia (AML) is a frequently diagnosed malignancy in adults. Long non-coding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1) has been well known to play vital roles in multiple malignancies including AML. Unfortunately, the detailed mechanism of CCAT1 in AML progression remains obscure. In this study, we demonstrated that CCAT1 was up-regulated in AML samples while its target, miR-490-3p, was relatively down-regulated. CCAT1 markedly increased viability and metastasis of AML cells, while miR-490-3p had opposite effects. CCAT1 could specifically bind to miR-490-3p and reduce its expression and activity, and MAPK1 was a target gene of miR-490-3p. Overexpressed CCAT1 could induce MAPK1 expression and c-Myc reciprocally increased CCAT1 expression. Our data implied that miR-490-3p could be a novel therapeutic target for AML, and highlights the crucial role of CCAT1/miR-490-3p/MAPK1/c-Myc positive feedback loop in AML progression.

LncRNA ANRIL promotes cell proliferation, migration and invasion during acute myeloid leukemia pathogenesis via negatively regulating miR-34a.

OBJECTIVE: LncRNA ANRIL (antisense non-coding RNA in the INK4 locus) was highly expressed in acute myeloid leukemia (AML) patients to promote AML pathogenesis. In this study, we aimed to investigate the roles and molecular events of ANRIL associated with AML progression. METHODS: Expression patterns of ANRIL and miR-34a in the bone marrow (BM) samples and cell lines were determined using qRT-PCR. Cell proliferation, apoptosis, migration and invasion of cells with ANRIL knockdown or miR-34a overexpression were assessed by CCK-8, EdU staining, flow cytometry and Transwell assays, respectively. The dual-luciferase reporter assay was employed to validate the relationship between miR-34a and Histone deacetylase 1 (HDAC1). The binding of E2 F1 (E2 F transcription factor 1) with gene promoter was analyzed by ChIP. Furthermore, the tumorigenicity of AML was determined by xenograft transplantation in nude mice. RESULTS: ANRIL was up-regulated both in the BM samples from AML patients and cell lines (HL-60 and THP-1), of which expression was negatively correlated with miR-34a expression. ANRIL knockdown inhibited cell proliferation, migration and invasion but promoted apoptosis of AML cells, while overexpression of miR-34a exerted opposite effects. miR-34a was verified as a downstream gene targeted by ANRIL. Moreover, HDAC1 was a direct target of miR-34a, and HDAC1 overexpression impaired the recruitment of E2 F1 to ASPP2 (apoptosis stimulating proteins of p53) gene promoter. ANRIL knockdown significantly inhibited the tumorigenesis of AML. CONCLUSION: ANRIL promotes AML development through HDAC1-mediated epigenetic suppression of ASPP2 via negatively regulating miR-34a, which might serve as a therapeutic target for AML treatment.

Correction: Risk factors for postoperative meningitis after microsurgery for vestibular schwannoma.

[This corrects the article DOI: 10.1371/journal.pone.0217253.].

Risk factors for postoperative meningitis after microsurgery for vestibular schwannoma.

OBJECTIVE: Meningitis after microsurgery for vestibular schwannoma (VS) is a severe complication that results in high morbidity. However, few studies have focused on meningitis after VS surgery. The purpose of this study was to identify the risk factors for meningitis after VS surgery. METHODS: We performed a retrospective analysis of all VS patients who underwent microsurgery and survived for at least 7 days after surgery, between 1 June 2015 and 30 November 2018 at West China Hospital of Sichuan University. Univariate and multivariate analyses were performed to identify the risk factors for postoperative meningitis (POM). RESULTS: We enrolled 410 patients, 27 of whom had POM. Through univariate analysis, the factors of hydrocephalus (p = 0.018), Koos grade IV (p = 0.04), operative duration > 3 hours (p = 0.03) and intraoperative bleeding volume ≥400 ml (p = 0. 02) were significantly correlated with POM. The multivariate analysis showed that Koos grade IV (p = 0.04; OR = 3.19; 95% CI 1.032-3.190), operation duration > 3 hours (p = 0.03; OR = 7.927; 95% CI 1.043-60.265), and intraoperative bleeding volume ≥ 400 ml (p = 0.02; OR = 2.551; 95% CI 1.112-5.850) were the independent influencing factors of POM. CONCLUSIONS: Koos grade IV, operation duration > 3 hours, and intraoperative blood loss ≥ 400 ml were identified as independent risk factors for POM after microsurgery for VS. POM also caused a prolonged hospital stay.

PELP1 is a novel oncogene in gastric tumorigenesis and negatively regulated by miR-15 family microRNAs.

BACKGROUD: Gastric cancer (GC) is one of the leading causes of cancer-related death in East Asia and some South American countries, but its mechanism has not been clarified clearly. Proline-, glutamic acid-, and leucine-rich protein-1 (PELP1), a co-regulatory molecule of estrogen receptor α (ER α), is up-regulated in series of cancers such as endometrial carcinoma, ovarian cancer, colorectal cancer, breast cancer, and non-small cell lung cancer. However, PELP1's role in GC is still obscure, and its aberrant expression in cancers also remains to be explained. METHODS: Immunohistochemical staining and Real-time PCR were used to compare the expression level of PELP1 in GC tissues and adjacent tissues. Western blot was used to detect the expression of PELP1 in cell lines. Kaplan-meier analysis and chi-square test were applied to evaluate the potential of PELP1 to function as a cancer biomarker. RNA interference was used to inhibit PELP1 expression in GC cells, followed by detecting cell proliferation, apoptosis, migration and invasion. Luciferase assay was conducted to validate whether miR-15 family members can directly target PELP1. RESULTS: In this study, we validated that PELP1 was significantly up-regulated in GC samples and cell lines. It was also demonstrated that the up-regulation of PELP1 was associated with several clinicopathologic features such as tumor diameter (P< 0.001), serum CEA level (P= 0.034), and lymphatic metastasis (P= 0.0009) of GC patients, and its high expression was correlated with shorter disease-free survival and overall survival of the patients. Knockdown of PELP1 remarkably arrested the proliferationï» migration and invasion, while promoted apoptosis. We also confirmed that miR-15 family microRNAs, most of which were down-regulated and tumor suppressor in cancers, were posttranscriptional regulators of PELP1. CONCLUSION: In conclusion, we demonstrated that PELP1 was an oncogene of GC associated with patients' prognosis and miR-15 family members contributed to its aberrant expression in cancers.

Risk Factors for Postoperative Intracranial Hemorrhage After Resection of Intracranial Tumor in 2259 Consecutive Patients.

BACKGROUND: Postoperative hemorrhage (POH), an uncommon complication after cranial operation, may result in prolonged postoperative hospitalization, severe neurologic impairment, or even death. Most models in studies detecting risk factors for POH include all kinds of cranial lesions; however, factors associated with POH may vary among intracranial diseases. There is a paucity of large sample studies focusing solely on POH after intracranial tumor surgery. Therefore, this study was designed to investigate the preoperative risk factors for POH after surgery for intracranial tumor. METHODS: Medical records of 2259 adult patients who underwent primary surgical resection of single intracranial tumor between January 2017 and June 2018 at West China Hospital of Sichuan University were retrospectively studied. Univariate and multivariate analyses were performed to identify the risk factors for POH after resection of intracranial tumor. RESULTS: POH (defined as postoperative hematoma requiring surgical evacuation) occurred in 40 of 2259 patients (1.8%). Univariate analysis revealed that older age (P = 0.037, Wilcoxon-Mann-Whitney test), higher international normalized ratio (INR) (P = 0.037, Wilcoxon-Mann-Whitney test), and larger tumor size (P = 0.001, Wilcoxon-Mann-Whitney test) were significantly associated with POH. Then it was confirmed by multivariate analysis that all of the 3 factors (older age: P = 0.033, higher INR: P = 0.044, larger tumor size: P = 0.002) were independent risk factors for POH after removal of intracranial tumor. CONCLUSIONS: Older age, higher INR, and larger tumor size were identified as independent risk factors for POH after resection of intracranial tumor in adults.