PLK1 plays a crucial role in cell cycle regulation and cancer development, and its dysregulation has been implicated in the prognosis of a variety of malignancies. The potential of PLK1 inhibitors as cancer therapeutics has been extensively investigated. However, the underlying biology and mechanisms of PLK1 remain incompletely understood. In recent years, numerous studies have demonstrated that PLK1 overexpression is associated with resistance to certain chemotherapeutic agents, while its inhibition can enhance the efficacy of chemotherapy. In addition, PLK1 inhibitors have been shown to selectively target cancer cells as radiation sensitizers and exert synergistic effects in combination immunotherapy. The underlying mechanisms may involve the regulation of multiple immune cells and inflammatory factors, as well as alterations in the tumor microenvironment, ultimately influencing tumor genesis, migration, and invasion. Moreover, PLK1 can regulate the expression of immune checkpoint-related proteins, thereby playing a synergistic role in cancer therapy. Furthermore, PLK1 represents a promising target antigen for cancer immunotherapy, with potential applications in optimizing cancer vaccines. Therefore, this review focuses on the applications and underlying mechanisms of PLK1 in tumor immunotherapy, aiming to provide new insights for improving patient outcomes and prognosis.

Background: Camrelizumab has become the first-line treatment for most patients with advanced tumors. Among advanced tumor patients undergoing camrelizumab, the majority develop immunogenicity, resulting in the production of anti-drug antibodies (ADA). The impact of ADA on the efficacy and safety of camrelizumab treatment is currently unknown. Method: Hematologic samples from 31 tumor patients treated with camrelizumab were collected to serve as an experimental cohort for ADA levels detection. Concurrently, a separate validation cohort consisting of 16 patients was established. Follow-up data on patients’ OS and PFS were collected and analyzed. Results: High ADA levels (≥1200 ng/ml) after the three cycles camrelizumab treatment were linked to poorer patient outcomes, as shown by significant differences between PD and PR (P = 0016) and PR and SD (P = .0439). This trend was also present in the validation cohort (PD vs PR, P = .0413). More importantly, high ADA levels after the three cycles camrelizumab treatment were associated with a significant reduction in OS (P = .0128) and PFS (P = .0004), with the validation cohort reporting comparable findings (OS: P = .0009; PFS: P = .0007). Additionally, camrelizumab concentration was negatively correlated with ADA levels (experimental cohort: R2 = 0.3876; validation cohort: R2 = 0.3702). Patients had higher ADA levels after the early phase of camrelizumab treatment. Conclusion: High ADA levels were associated with shorter OS and PFS in patients after three cycles of camrelizumab therapy. Furthermore, patients had higher ADA levels after the early phase of treatment, specifically in the first three cycles with camrelizumab. It found that the higher the ADA concentration, the lower the serum camrelizumab concentration.

Objectives: This study aimed to determine the cutoff value for diagnosis and predict mortality in hepatocellular carcinoma (HCC) based on serum total superoxide dismutase (SOD) activity. Methods: A retrospective case-control study of the SOD Model was conducted using data from a single-center dataset at Shandong Provincial Hospital Affiliated with Shandong First Medical University, China. Serum total SOD activity was analyzed in HCC patients (n = 124) and control subjects (n = 117). Receiver operating characteristic (ROC) curves were used to determine cutoff values of serum total SOD activity for HCC diagnosis. Overall survival (OS) was assessed using the Kaplan-Meier method. Results: In the model groups, the cutoff level of total SOD activity for HCC was 169.2 U/mL (sensitivity: 87.23%, specificity: 91.95%), while for HCC [alpha fetoprotein (AFP) < 20 ng/mL], it was 173.4 U/mL (sensitivity: 86.79%, specificity: 88.51%). Additionally, in the validation groups, the true positive rate, true negative rate, and accuracy rate were all above 90%. Based on the cutoff value of SOD, HCC patients were assigned to an H-SOD and L-SOD group depending on their serum total SOD activity at admission before operation. The 5-year OS rate of the H-SOD group was 75.00%, and that of the L-SOD group was 36.59% in HCC patients (P = 0.0245). With a decrease in SOD activity, serum levels of Zn (t = 3.890, P = 0.0003) and Se (t = 7.694, P < 0.0001) were also significantly decreased and positively correlated with SOD activity (both P < 0.05) in HCC patients. Conclusions: Low serum total SOD activity may also be a risk factor for HCC. The decrease of SOD activity in HCC patients was partly related to a lack of Zn and Se.

Background:Oxidative stress is one risk factor for hepatocellular carcinoma (HCC). Oxide dismutase (SOD) is an important index to evaluate oxidative stress process. However, the cut-off value of diagnosis and the prediction of mortality in hepatocellular carcinoma (HCC) based on serum total SOD activity are unclear.Methods:Serum total SOD activity were analyzed in HCC patients (n = 124) and control subjects (n = 117). Mn, Fe, Cu, Zn and Se were detected by limiting dilution method using Agilent 7900 Inductively Coupled Plasma Mass spectrometry (ICP-MS). Receiver operating characteristic (ROC) curves was used to determine cutoff values of serum total SOD activity for the diagnosis of HCC. Overall survival (OS) were determined via the Kaplan-Meier method.Results:In model groups, the cut-off level of total SOD activity for HCC was 169.2 U/mL (Sensitivity:87.23%, Specificity:91.95%), while for HCC (AFP<20 ng/ml) it was 173.4 U/mL (Sensitivity:86.79%, Specificity:88.51%). Additionally, in the validation groups, the true positive rate, the true negative rate and the accuracy rate were all above 90%. According to the cutoff value of SOD, the HCC patients were assigned to an H-SOD and L-SOD group depending on their serum total SOD activity at admission before operation. The 5-year overall survival (OS) rate of the H-SOD group was 75.00% and that of the L-SOD group 36.59% in HCC patients (p=0.0245). Accompanied by a decrease in SOD activity, the serum levels of Zn (t=3.890, p=0.0003) and Se (t=7.694, p<0.0001) were also signifificantly decreased and correlated positively with SOD activity (both p<0.05) in HCC patients.Conclusions:Low serum total SOD activity may also be a risk factor for HCC. HCC patients with low serum total SOD activity might have poor prognoses for survival. The decrease of SOD activity in HCC patients was partly related to a lack of Zn and Se.

Heat stroke is a life-threatening heat-related emergency that often leads to multiple organ dysfunction syndrome (MODS), with liver injury among its most prominent manifestations. HS-associated acute liver injury (HS-ALI) is a major determinant of prognosis, yet its pathogenesis remains incompletely understood. Current evidence suggests that HS-ALI results from the interplay of direct thermal stress, systemic inflammation, oxidative imbalance, coagulation dysfunction, and regulated cell death. Emerging experimental studies have implicated pyroptosis, ferroptosis, necroptosis, and gut–liver immune crosstalk in HS-associated tissue injury; however, the strength of evidence varies considerably among these mechanisms, and direct validation in human HS-ALI remains limited. Accordingly, these pathways should be considered potential contributors to disease progression rather than uniformly established mechanisms.