Accumulating evidence suggests that intrinsic resistance to radiotherapy reduces the survival of patients with cancer. The present study investigated whether miR-93-5p affects proliferation, migration, apoptosis, and radiosensitivity of breast cancer (BC) cells. MDA-MB-468, MCF-7, and MDA-MB-231 BC cells were incubated with hsa-miR-93-5p mimics, hsa-miR-93-5p inhibitor, and negative control RNA with or without exposure to ionizing radiation to determine cell proliferation, migration, and apoptosis using the Cell Counting Kit-8 assay, wound healing assay and apoptotic assay, respectively. Overexpression of miR-93-5p inhibited the migratory abilities (P = 0.001) and decreased the cell proliferation (P = 0.049) of MCF-7 cells. In MCF-7 cells, a significant increase in apoptosis was detected after treatment with miR-93-5p compared with the negative control (P = 0.001) and miR-93-5p inhibitor (P = 0.004). In MDA-MB-468 cells, the proportion of apoptotic cells increased following exposure to ionizing radiation (P = 0.001). The percentage of apoptotic MDA-MB-231 cells in the miR-93-5p group was significantly increase compared with that determined in the negative control (P = 0.044) and hsa-miR-93-5p inhibitor (P = 0.046) groups. In conclusion, our findings showed that miR-93-5p reduces BC cell proliferation and migratory capacity, and increases the ratio of apoptotic cells. Overexpression of miR-93-5p could increase radiosensitivity in BC cells by increasing apoptosis. This evidence provides new insight into the treatment of BC and identifies miR-93-5p as a potential therapeutic target.

Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic options. Ferritinophagy, an autophagy‐dependent process regulating iron metabolism, has emerged as a key contributor to ferroptosis and tumour progression. This study hypothesised that the ferritinophagy‐related gene FTH1 drives HCC pathogenesis by modulating tryptophan metabolism and reactive oxygen species (ROS)‐dependent ferroptosis. To test this, we first analysed TCGA data to identify prognostic ferritinophagy genes, revealing FTH1 as a critical risk factor. Functional experiments using FTH1 ‐knockdown/−overexpressing HCC cell lines and xenograft models demonstrated that FTH1 enhances proliferation, migration, and tumour growth by upregulating CYP1A1/CYP1A2 in the tryptophan pathway, thereby increasing the synthesis of 6‐hydroxymelatonin (6‐HMT). Mechanistically, 6‐HMT suppressed ROS and ferroptosis by inhibiting cytochrome P450 oxidoreductase (POR). Concurrently, intracellular tryptophan levels were found to inhibit NCOA4‐mediated selective autophagy of FTH1, stabilising FTH1 levels and promoting tumour survival. Collectively, our findings establish FTH1 as a central regulator of ferritinophagy in HCC and reveal its dual role in linking tryptophan metabolism to redox homeostasis. This result provides a hint of how FTH1 influences HCC pathogenesis and positions the tryptophan metabolism pathway as a promising therapeutic target.

Breast cancer (BC) is the most common type of cancer in women. Triple‑negative BC (TNBC) constitutes 10‑15% of all BC cases and is associated with a poor prognosis. It has previously been reported that microRNA (miR)‑93‑5p is dysregulated in plasma exosomes from patients with BC and that miR‑93‑5p improves radiosensitivity in BC cells. The present study identified EphA4 as a potential target gene of miR‑93‑5p and investigated the pathway related to miR‑93‑5p in TNBC. Cell transfection and nude mouse experiments were performed to verify the role of the miR‑93‑5p/EphA4/NF‑κB pathway. Moreover, miR‑93‑5p, EphA4 and NF‑κB were detected in clinical patients. The results revealed that EphA4 and NF‑κB were downregulated in the miR‑93‑5p overexpression group. By contrast, EphA4 and NF‑κB expression levels were not significantly altered in the miR‑93‑5p overexpression + radiation group compared with those in the radiation group. Furthermore, overexpression of miR‑93‑5p with concomitant radiation therapy significantly decreased the growth of TNBC tumors in vivo. In conclusion, the present study revealed that miR‑93‑5p targeted EphA4 in TNBC through the NF‑κB pathway. However, radiation therapy prevented tumor progression by inhibiting the miR‑93‑5p/EphA4/NF‑κB pathway. Therefore, it would be interesting to elucidate the role of miR‑93‑5p in clinical research.

Background: Urothelial carcinoma is a major subtype of bladder cancer and small cell carcinoma (SCC) is a rare type of cancer in clinical practice. Pathologic collision of urinary bladder urothelial carcinoma with SCC is not common in clinical settings. Case presentation: Here, we report a patient with high-grade papillary carcinoma which changed to collision tumor with SCC. The patient underwent radical cystectomy; however, neck and mediastinum lymph nodes metastases were detected 11 months after the operation. The lymph nodes were diagnosed pathologically as SCC. Chemoradiotherapy was subsequently prescribed. Unfortunately, this patient died of COVID-19 in early 2023. Discussion: We hypothesized the mechanism underlying this pathological transformation. For patients with urothelial bladder cancer, pathological analysis should be conducted to allow standardized and persistent treatment. Moreover, drugs should be selected depending on the type of pathology, especially for patients who develop relapse, since collision tumor or other pathological tumors may be present. Conclusions: We recommend that radical cystectomy be performed early enough for patients with non-muscle invasive bladder cancer, who are at a high risk of tumor recurrence. However, this conclusion needs to be validated in a larger number of patients.

Background: The long noncoding RNA (lncRNA) GAPLINC, or gastric adenocarcinoma predictive long intergenic ncRNA, plays a carcinogenic role in a variety of different tumor types. There is limited information regarding the biological function of GAPLINC in the development of esophageal squamous cell carcinoma (ESCC). Methods: Surgical tissue samples of 40 patients undergoing ESCC radical surgery were collected, including ESCC tissues and corresponding adjacent normal tissues. Quantitative real-time PCR (qRT-PCR) was used to detect the expression of lncRNA GAPLINC in the human ESCC cell line (TE11). The function role of LncRNA GAPLINC was detected after specific siRNA interference and overexpression in the TE11 cell line. The effects of LncRNA GAPLINC on ESCC cell proliferation, migration and invasion abilities were investigated by flow cytometry, using the Cell Counting Kit-8 (CCK-8), and by Transwell migration assays, respectively. Results: The expression of lncRNA GAPLINC in ESCC tissues was significantly higher than that in corresponding adjacent normal tissues (P< 0.05) and correlated with the degree of tumor differentiation (P< 0.05). Compared with human esophageal normal epithelial cell lines, the expression of LncRNA GAPLINC was significantly higher in the human ESCC cell line (P< 0.05). CCK-8 assays showed that LncRNA GAPLINC overexpression increased the growth rate of cells (P< 0.05). Transwell experiments showed that LncRNA GAPLINC overexpression increased the ability of cell migration and invasion compared to control cells (P< 0.05). Annexin V assay revealed that LncRNA GAPLINC silencing increased early stage apoptosis (P< 0. 05). Conclusion: Our results suggest that LncRNA GAPLINC may be used as a biomarker for the diagnosis and monitoring of ESCC, and may play an oncogenic role in ESCC.

Objective: This study examined the potential risk value of the serum albumin to globulin ratio (AGR) in patients with breast cancer (BC). Methods: This study employed a retrospective design, enrolling 332 patients with BC and 38 patients without BC treated at Taizhou People’s Hospital between September 2015 and May 2021. Multivariate Cox proportional hazard regression models were used to identify potential risk factors. A prognostic nomogram was developed based on the multivariate analyses. The receiver operating characteristic curve determined the optimal cutoff value for AGR. Results: The results indicated a statistically significant decrease in AGR among patients with BC. Significant disparities were observed in globulin and AGR levels between the two cohorts. AGR was significantly associated with tumor size and stage, with a marked decline in advanced stages of BC. Additionally, AGR and aspartate transaminase/Alanine aminotransferase (AST/ALT) emerged as significant diagnostic indicators for invasive carcinoma and advanced stages (II–IV) of BC. Specifically, AGR exhibited an area under the curve of 0.645 (P < 0.003), highlighting the discriminatory capacity of serum globulin levels in distinguishing between BC and non-BC cohorts. Conclusions: The AGR, routinely assessed due to its simplicity, objectivity, and cost-effectiveness, holds promise as a potential risk factor for BC and may have practical implications in clinical settings.