TP53 expression

In vivo experiments showed that Obacunone effectively inhibited tumor growth. Obacunone exhibits potential therapeutic significance through the modulation of the Akt/p53 signaling pathway, which may induce ferroptosis and inhibit the proliferation of ovarian cancer cells.

p21-dependent quiescence exists in TP53 wild-type NSCLC cells and provides survival advantages to these cells. Targeting p21 function in TP53 wild-type tumours could lead to better outcomes for chemotherapy treatment in NSCLC patients.

Our results advocate for the potential of metformin as a viable therapeutic option for preserving ovarian function in cyclophosphamide-treated adolescent girls, given its favorable side effect profile and ability to improve cyclophosphamide-induced ovarian damage.

In addition, ALG-12 inhibited the transcription of ataxia-telangiectasia mutated-and Rad3-related gene(ATR), tumor protein p53 gene(Tp53), Bcl-2 binding component 3 gene(BBC3), and Bcl-2 associated X protein gene(Bax) in the p53 signaling pathway, decreased the protein expression levels of p53, Bax, and cleaved caspase-3, and increased the protein expression levels of B-cell lymphoma/leukemia 2(Bcl-2) and caspase-3. The results suggested that ALG-12 had a protective effect on DDP-induced renal tubular epithelial cell injury, and the mechanism may be related to the inhibition of p53-mediated apoptosis, which provided a basis for further development of ALG-12.

TERT mutation was present in the oligodendroglioma component, whereas it was absent in the astrocytoma component. Although rare, gliomas harboring both oligodendroglioma and astrocytoma components in a single tumor exist and show genetically distinct areas.

We detected 160 alterations with potential treatment implications, with 21.2% of samples showing alterations in the homologous recombination pathway. To the best of our knowledge, this study describes the largest cohort of pSCC with complex molecular-pathological, clinical, and prognostic analysis correlating with prognosis.

Moreover, ML385 was found to reduce the expression of LDHA, glucose uptake, and the levels of lactate derived from glycolysis. Overall, these results suggest that Nrf2 functions as an oncogene in ATL and may represent a promising therapeutic target.

An increase in the expression of the CDKN2A gene was also observed when PBMCs were exposed to PS-NPs with 29 nm in diameter at the highest concentration. The observed effect depended on both the concentration and the size of the PS-NPs.

After 96 h from inhibitor removal, the G361 line presented signs of senescence (increased level of SA-β-galactosidase, IL-8, P-P53, G2/M and S phases of cell cycle, decreased lamin B1 and cleaved lamin B1), while the A375 line demonstrated more signs of apoptosis (increased subG1 phase, P-P53, cleaved lamin B1). The gathered findings suggest that MZB resulted in the induction of cellular senescence (line G361) or enhanced apoptosis (line A375) in the melanoma cell lines tested here and could be a promising therapeutic factor in malignant melanoma treatment.

PDT represents a powerful and versatile treatment option for various dermatological conditions due to its ability to target cellular pathways involved in proliferation and apoptosis. Further research into optimizing treatment parameters and combining PDT with other targeted therapies may enhance patient outcomes, reduce resistance, and pave the way for more individualized therapeutic approaches in dermatology.

HMM has potential therapeutic effects on the liver cancer. This study provides important insights regarding the methods for investigating HMM in the treatment of hepatocellular cancer.

Furthermore, the incidence of abnormal 53BP1 expression in cancer cells was higher than in non-neoplastic epidermal cells surrounding cancer, suggesting a correlation between the type of 53BP1 and the malignant potential of skin tumors. This study highlights the usefulness of dual-color IF for 53BP1 (and Ki-67) as an indicator to estimate the level of GIN as a long-lasting health effect of radiation exposure.

The findings from this study address the noteworthy antiproliferative effects of PR-AgNPs in cancer cells primarily mediated through activation of intrinsic apoptosis pathway by inducing p53 and caspase-3 genes.

Our findings emphasized that the combinatorial therapy of sericin and HQ could orchestrate the PI3K/Akt/Nrf2/NF-κB signaling pathway in the lungs, counteracting oxidative stress, inflammation, and uncontrolled cellular proliferation and sustaining lung structures. Furthermore, they could serve as anticancer agents, hindering lung cancer progression.

For diagnostic purposes, taking into account, Rb status improved, but only marginally, the performances of p53 status. In conclusion, our study underlines the molecular heterogeneity of NET-G3 and LCNEC, irrespectively of the primary, and provides further insight on the diagnostic relevance of p53/Rb immunodetection in high-grade neuroendocrine neoplasms.

Tumors with p53 abnormal expression and absence of p16 showed a greater DOI. Our data suggest an association between PDL1 expression and increased inflammatory infiltrates in vulvar SCC.

This study emphasizes the importance of personalized approaches in the use of MAL-PDT, tailoring treatment according to tumor-specific characteristics. Biomarkers such as p53, β-catenin, and GLUT1 can serve as predictive tools for PDT response, helping clinicians identify patients who may benefit from alternative or combined treatments to enhance therapeutic efficacy.

CD47 and CTLA-4 expressions can be considered possible diagnostic and prognostic markers in EC. They were good markers of P53 mutation, and higher tumor grades and stages.

RRx-001 reduces the viability of HCC cells and induces apoptosis. This effect may be due to the downregulation of CD47 expression and the alteration of the TP53 protein regulatory pathway.

Using a cut-off set at 30% expression of neoplastic cells, we noted an overexpression of p53 in T-MF and T-SS compared with nontransformed forms (47% vs. 12%, respectively, P < 0.01) and in MF compared with SS (23% vs. 7%, respectively, P < 0.01). Overexpression of p53 with a cut-off at 30% therefore seems to be a discriminating tool in the differential diagnosis of MF/SS versus their transformed forms as well as the differential diagnosis between MF and SS.

MCF7 cells also show reduced necroptosis and increased necrosis. These findings highlight that H2pmen induces varied cytotoxic effects across MDA and MCF7 cells, with MDA cells exhibiting more pronounced apoptosis and necroptosis alongside complex anti-apoptotic responses.

Specifically, TOE1 up-regulated p53 expression by enhancing p53 promoter activity, and up-regulated p21 expression by enhancing p21 mRNA stability. Collectively, our findings first contribute to further elucidating the molecular mechanisms by which TOE1 participates in the regulation of gastric cancer progression, and are expected to provide a theoretical basis for diagnosis and targeted treatment of gastric cancer.

These findings underlined that MA has anti-EC potential by modulating multiple targets including PLA2G10, PDE4D, and PDE5A, inhibiting EC cell proliferation, inducing G2/M phase arrest, and causing metabolic shifts. This study provides theoretical support for advanced experimental research on its clinical applications.

Moreover, KRAS expression was shown to be significantly associated with perineural invasion (p = 0.005). This is the first study that investigates protein biomarker expression in a large cohort of Pakistani PDAC patients. The findings from the study may provide directions about the population specific biomarkers and targeted therapies for these patients.

Up-regulated of P53, SLC7A11 and GPX4 expression, and inhibited expression of PTGS2. PMZ regulates the SLC7A11-GPX4 antioxidant system to protect hippocampal neurons from oxidative stress injury.

Once a gastric-type phenotype is confirmed, mutation surrogate immunostains can be used to support a diagnosis of GAS. PD-L1 and HER2 expression is seen in a subset of GAS offering therapeutic options for this aggressive tumor.

Sonodynamic therapy in inertial acoustic cavitation threshold, combined with ionizing radiation in the presence of biocompatible nanoparticles, could enhance the therapeutic effects on the miR-1204, derived from lncRNA PVT1, that functions as an oncogenic microRNA in breast cancer. This approach has the potential to overcome treatment resistance encountered with single therapies.

As per the research described above, lung cancer cells were effectively targeted by the anticancer and antioxidant abilities of ZnO nanoparticles inspired by Betanin (A549).

Pathologists without gynecologic subspecialty expertise benefited the most from a brief educational module, which fostered a better understanding and improved comfort level with the p16/p53 stain interpretation and tumor pathway designation in the diagnosis of vSCC. Some interpretative challenges remain, particularly in regard to select p53 patterns and high-risk HPV-in situ hybridization utilization, warranting additional research.

Compared to traditional prediction models, the model proposed in this study that combined molecular indicators and clinicopathologic parameters can better predict the prognosis of EC patients.

The formation of TLS may play a significant role in inhibiting lymph node metastasis, liver metastasis, and vascular tumor thrombus in colorectal cancer, and patients with mature TLS have a favorable clinical prognosis, which can provide a reference for the immunotherapy and prognostic assessment of colorectal cancer patients.

On the other hand, silencing Orp53 expression via siRNA resulted in significant reductions in CNS cell viability (P < 0.05). Our study establishes a molecular basis for evaluating the consequences of marine noise pollution, confirming that low-frequency noise activates the p53 signaling pathway, oxidative stress, and that p53 can regulate oxidative stress and apoptosis-related genes.

We further demonstrated that C-30 impaired tumor growth and increased the expression of p53-target genes in vivo. These results suggested that C-30 produces tumor-suppressive effects similar to the functional reactivation of p53, providing a rationale for the inhibition of PSF activity as a promising therapy against treatment-resistant cancer.

In vivo, we demonstrated that 50 mg/kg MA significantly inhibited the growth of tumors established using RM-1 cells. To summarize, we report that MA inhibits prostate cancer cell growth both in vitro and in vivo by inducing autophagy and ferroptosis via transcriptomic and metabolomic reprogramming.

The reference drug (Doxorubicin) showed a higher toxicity against Vero CCL-81(IC50: 0.41 μg/mL) and DU-145 (IC50: 0.28 μg/mL) cells and a lower selectivity index of 1.46. The DU-145 cells treated with the studied plant extracts exhibited notable upregulation of ar and bcl2, and normalization of caspase 3, cdk1 and p53 expression. The studied plant extracts possess in vitro anti-prostate cancer properties and could be promising candidates for further preclinical studies aimed at developing novel botanical-based therapies for the management of prostate cancer.

Despite the retrospective nature and variations in immunohistochemistry reporting, our study provides valuable insights into patient outcomes, particularly in a demographically diverse population. Future research, like the STRIVE trial, may determine if implementation of p16 and p53 stratified management algorithm will improve outcomes for women with vulvar SCC (McAlpine, 2024).

Furthermore, p53 expression in human subcutaneous and visceral WAT correlated positively with BMI, whereas its expression in visceral WAT was inversely associated with insulin sensitivity (as assessed by hyperinsulinemic-euglycemic clamp). Taken together, our data suggest that Fas regulates p53 expression in adipocytes, and may thereby affect body weight gain and insulin sensitivity.

HMA induced apoptosis in HepG2 cells, while inhibiting proliferation and invasion. The mechanism of HMA against HCC may be related to the SIRT1/p53 pathway.

Our study supports full molecular classification of UCS. We also raise awareness for potentially assessing POLE mutation allele fraction and clonality in the consideration of classifying a tumor as POLEmut.

Our study provides a novel understanding of the role of complex I in lipid reprogramming facilitating colon cancer invasion and metastasis.

In high-risk HPV-positive CC patients, HPV seems to play a role in recurrent disease. Our findings support ongoing research on targeting HPV oncogenes in CC, also in metastatic disease.

In conclusion, this study emphasizes the potential of AMO-mediated splice correction as a therapeutic approach for TP53 mutations. &lsqb;BMB Reports 2024; 57(11): 503-508].