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Background: The improvements in the treatment of colorectal cancer (CRC) and prolongation of survival time have improved the incidence of bone metastasis. Forkhead box D3 (FOXD3) is involved in the development of CRC. However, the role and mechanism of FOXD3 in CRC bone metastases development are unknown. Objective: Using the combined bioinformatics and cytology experimental analyses, this study aimed to explore the mechanistic role of FOXD3 in the bone metastasis of colon cancer, thereby aiding in the treatment of colon cancer bone metastasis and identification of drug-targeting markers. Methods: First, the changes in the expression levels of the FOXD3 gene and differentially expressed genes (DEGs) between the colon cancer samples and colon cancer metastases were obtained from The Cancer Genome Atlas (TCGA) database. Then, the correlations of the FOXD3 gene with the DEGs were identified. Next, the effects of the FOXD3 on the proliferation and invasion abilities of colon cancer bone metastatic cells were identified using Cell Counting Kit-8 (CCK8) and Transwell cell migration assays, respectively. In addition, Western blot analysis was used to identify the expression levels of the proteins related to the EGFR/Ras/Raf/MEK/ERK(EGFR/ERK) signaling pathway and epithelial-to-mesenchymal transition (EMT). Results: FOXD3 was downregulated in colon cancer and could interact with multiple DEGs in colon cancer bone metastases. FOXD3 gene knockdown could increase the proliferation of human colon cancer bone metastatic cells and their invasive ability. FOXD3 gene knockdown could activate the expression of EGFR/ERK signaling pathway-related proteins and inhibit/promote the expression of EMT-related proteins, which in turn promoted the proliferation and metastasis of LoVo cells from colon cancer bone metastases. Conclusion: Overall, this study demonstrated that the downregulation of the FOXD3 gene might promote the proliferation of colon cancer bone metastatic cell lines through the EGFR/ERK pathway and promote their migration through EMT, thereby serving as a promising therapeutic target.

Although the National Comprehensive Cancer Network (NCCN) guidelines include clear recommendations for the appropriate resection margins in non-acral cutaneous melanoma, the required margin for acral melanoma is controversial. In this retrospective study, we aimed to investigate whether narrow-margin excision is warranted for thick acral melanoma. Records from 277 melanoma patients with stage T3–T4 disease who underwent radical surgery in three centers in China from September 2010 to October 2018 were reviewed. Clinicopathologic data, including age, gender, excision margin (1–2 cm versus ≥ 2 cm), Clark level, Breslow thickness, ulceration, N stage and adjuvant therapy, were included for survival analysis. The patients were followed up until death or March 31, 2021. Log-rank and Cox regression analyses were used to identify prognostic factors for overall survival (OS), disease-free survival (DFS) and local and in-transit recurrence-free survival (LITRFS). Among all enrolled patients, 207 (74.7%) had acral melanoma, and 70 (25.3%) had non-acral cutaneous melanoma. No significant difference in baseline characteristics was identified between non-acral and acral melanoma, except for age (p = 0.004), gender (p = 0.009) and ulceration (p = 0.048). In non-acral melanoma, a resection margin of 1–2 cm was a poor independent prognostic factor for OS [p = 0.015; hazard ratio (HR) (95% CI), 0.26 (0.009–0.77)] and LITRFS [p = 0.013; HR (95% CI), 0.19 (0.05–0.71)] but not for DFS [p = 0.143; HR (95% CI), 0.51 (0.21–1.25)]. Forty-three (20.8%) patients in the acral melanoma group had a 1–2-cm resection margin. The resection margin was not correlated with patients’ OS (p = 0.196 by log-rank analysis, p = 0.865 by multivariate survival analysis), DFS (p = 0.080 by log-rank analysis, p = 0.758 by multivariate survival analysis) or LITRFS (p = 0.354 by log-rank analysis) in acral melanoma. As recommended in the NCCN guidelines, a resection margin ≥ 2 cm is required for non-acral cutaneous melanoma. Meanwhile, a narrow resection margin (1–2 cm) may be safe for patients with acral melanoma.

This study aimed to summarise the clinical experience of peritoneal tuberculosis (TB). Clinical data of 26 patients admitted and diagnosed with peritoneal TB mimicking advanced ovarian cancer or peritoneal carcinoma between June 2008 and June 2017, was evaluated. The mean age was 35.92 ±15.30 years. The most common findings were abdominal mass (n=21, 80.77%) and elevated CA 125 levels (n=19, 73.08%). One patient underwent PET-CT and was diagnosed with peritoneal TB. Laparotomy was performed in 14 patients (70%) and laparoscopy in six patients (30%), out of whom two patients were converted to laparotomy due to severe adhesions. Meanwhile, mass puncture biopsy or small incision biopsy was the preferred method for diagnosing peritoneal TB, while PET-CT was considered as a good diagnostic method.

BACKGROUND The aim of this study was to investigate the expression of a novel long noncoding RNA (lncRNA), LL22NC03-N64E9.1, and its effect on the phenotype of lung cancer cells and tissues using The Cancer Genome Atlas (TCGA) RNA sequencing data and other publicly available profiling data. MATERIAL AND METHODS The lung cancer dataset GSE30219 was downloaded from the Gene Expression Omnibus (GEO) repository. Differentially expressed lncRNA, LL22NC03-N64E9.1, in 48 lung cancer tissue samples and adjacent normal lung tissues, normal lung cell lines BEAS-2B and A549, and lung cancer cell lines, H1703, and H292, were detected by quantitative reverse transcription polymerase chain reaction (PCR) (qRT-PCR). Interference efficiency was performed using small interfering RNA (siRNA). Tumor levels of lncRNA, LL22NC03-N64E9.1, and clinicopathological parameters were statistically analyzed. RESULTS Analysis of the GSE30219 test cohort showed that lncRNA, LL22NC03-N64E9.1 expression was significantly increased in lung cancer. In clinical tissue samples, the level of LL22NC03-N64E9.1 in patients with lung cancer was significantly increased compared with adjacent normal lung tissues (P0.001). The level of LL22NC03-N64E9.1 in patients with lung cancer was significantly correlated with tumor size and TNM stage (P0.05), but not with age, sex and the presence of lymph node metastasis (P0.05). In the H292 cells, following knockdown of LL22NC03-N64E9.1, cell proliferation and cloning were reduced. CONCLUSIONS Expression of lncRNA, LL22NC03-N64E9.1, promoted proliferation of lung cancer cells in vitro, was highly expressed in lung cancer tissues and was associated with increased overall survival (OS), tumor size, and tumor stage in patients with lung cancer.