Ferritinophagy, a form of autophagy, is also an important part of ferroptosis, a type of regulated cell death resulting from abnormal iron metabolism involving the production of reactive oxygen species. As ferroptosis, autophagy and cancer have been revealed, ferritinophagy has attracted increasing attention in cancer development. In this review, we discuss the latest research progress on ferroptosis, autophagy-associated ferroptosis led by ferritinophagy, the regulators of ferritinophagy and promising cancer treatments that target ferritinophagy. Ferritinophagy is at the intersection of ferroptosis and autophagy and plays a significant role in cancer development. The discussed studies provide new insights into the mechanisms of ferritinophagy and promising related treatments for cancer.

Breast cancer (BC) is the world’s second most frequent malignancy and the leading cause of mortality among women. All in situ or invasive breast cancer derives from terminal tubulobular units; when the tumor is present only in the ducts or lobules in situ, it is called ductal carcinoma in situ (DCIS)/lobular carcinoma in situ (LCIS). The biggest risk factors are age, mutations in breast cancer genes 1 or 2 (BRCA1 or BRCA2), and dense breast tissue. Current treatments are associated with various side effects, recurrence, and poor quality of life. The critical role of the immune system in breast cancer progression/regression should always be considered. Several immunotherapy techniques for BC have been studied, including tumor-targeted antibodies (bispecific antibodies), adoptive T cell therapy, vaccinations, and immune checkpoint inhibition with anti-PD-1 antibodies. In the last decade, significant breakthroughs have been made in breast cancer immunotherapy. This advancement was principally prompted by cancer cells’ escape of immune regulation and the tumor’s subsequent resistance to traditional therapy. Photodynamic therapy (PDT) has shown potential as a cancer treatment. It is less intrusive, more focused, and less damaging to normal cells and tissues. It entails the employment of a photosensitizer (PS) and a specific wavelength of light to create reactive oxygen species. Recently, an increasing number of studies have shown that PDT combined with immunotherapy improves the effect of tumor drugs and reduces tumor immune escape, improving the prognosis of breast cancer patients. Therefore, we objectively evaluate strategies for their limitations and benefits, which are critical to improving outcomes for breast cancer patients. In conclusion, we offer many avenues for further study on tailored immunotherapy, such as oxygen-enhanced PDT and nanoparticles.

Background: As the major microtubule organizing center in animal cells, the centrosome is implicated with human breast tumor in multiple ways, such as promotion of tumor cell immune evasion. Here, we aimed to detect the expression of centrosome-related genes (CRGs) in normal and malignant breast tissues, and construct a novel centrosome-related prognostic model to discover new biomarkers and screen drugs for breast cancer.Methods: We collected CRGs from the public databases and literature. The differentially expressed CRGs between normal and malignant breast tissues were identified by the DESeq2. Univariate Cox and LASSO regression analyses were conducted to screen candidate prognostic CRGs and develop a centrosome-related signature (CRS) to score breast cancer patients. We further manipulated and visualized data from TCGA, GEO, IMvigor210, TCIA and TIMER to explore the correlation between CRS and patient outcomes, clinical manifestations, mutational landscapes, tumor immune microenvironments, and responses to diverse therapies. Single cell analyses were performed to investigate the difference of immune cell landscape between high- and low-risk group patients. In addition, we constructed a nomogram to guide clinicians in precise treatment.Results: A total of 726 CRGs were collected from the public databases and literature. PSME2, MAPK10, EIF4EBP1 were screened as the prognostic genes in breast cancer. Next, we constructed a centrosome-related prognostic signature and validated its efficacy based on the genes for predicting the survival of breast cancer patients. The high-risk group patients had poor prognoses, the area under the ROC curve for 1-, 3-, and 5-year overall survival (OS) was 0.77, 0.67, and 0.65, respectively. The predictive capacity of CRS was validated by other datasets from GEO dataset. In addition, high-risk group patients exhibited elevated level of mutational landscapes and decreased level of immune infiltration, especially T and B lymphocytes. In terms of treatment responses, patients in the high-risk group were found to be resistant to immunotherapy but sensitive to chemotherapy. Moreover, we screened a series of candidate anticancer drugs with high sensitivity in the high-risk group.Conclusion: Our work exploited a centrosome-related prognostic signature and developed a predictive nomogram capable of accurately predicting breast cancer OS. The above discoveries provide deeper insights into the vital roles of the centrosome and contribute to the development of personalized treatment for breast cancer.

Breast cancer (BC) is the most prevalent tumour in women worldwide. USP30 is a deubiquitinase that has been previously reported to promote tumour progression and lipid synthesis in hepatocellular carcinoma. However, the role of USP30 in breast cancer remains unclear. Therefore, we investigated its biological action and corresponding mechanisms in vitro and in vivo. In our study, we found that USP30 was highly expressed in breast cancer samples and correlated with a poor patient prognosis. Knockdown of USP30 significantly suppressed the proliferation, invasion and migration abilities of BC cells in vitro and tumour growth in vivo, whereas overexpression of USP30 exhibited the opposite effect. Mechanistically, we verified that USP30 interacts with and stabilises Snail to promote its protein expression through deubiquitination by K48-linked polyubiquitin chains and then accelerates the EMT program. More importantly, USP30 reduced the chemosensitivity of BC cells to paclitaxel (PTX). Collectively, these data demonstrate that USP30 promotes the BC cell EMT program by stabilising Snail and attenuating chemosensitivity to PTX and may be a potential therapeutic target in BC.

This investigation seeks to scrutinize the relationships between body composition metrics and the clinical outcomes observed in patients with cholangiocarcinoma (CCA). A comprehensive exploration was conducted across three prominent online databases: Embase, PubMed, and the Cochrane Library. This endeavor spanned the entirety of each database up to the cutoff date of September 29, 2023. To evaluate the quality of the included studies, the Newcastle-Ottawa scale was employed. This comprehensive analysis included a total of 26 articles with a combined patient cohort of 4398 individuals. The results demonstrated that CCA patients with low skeletal muscle index (SMI) had significantly inferior OS (HR: 1.93, p < 0.001) and RFS (HR: 2.02, p < 0.001), as well as a higher incidence of postoperative complications (OR: 1.69, 95% CI: 1.20–2.38, p < 0.001) compared to those with high SMI. The presence of sarcopenia in CCA patients was significantly related to poorer OS (HR: 1.96, p < 0.001) and RFS (HR: 2.05, p < 0.001), and a higher rate of postoperative complications (OR: 1.39, p = 0.049) in comparison to those without sarcopenia. Moreover, lower psoas muscle index (PMI) and myosteatosis were associated with shorter OS (PMI, HR: 1.56, p < 0.001; myosteatosis, HR: 1.49, p = 0.001) and RFS (PMI, HR: 2.16, p < 0.001; myosteatosis, HR: 1.35, p = 0.023). Our findings highlight incorporating body composition screening into clinical practice can help develop treatment strategies and optimize perioperative care, potentially improving patient outcomes.