Oncology reports最新文献

Bladder cancer is the most common malignant tumor of the urinary system with high morbidity and no clear pathogenesis. The Hippo signaling pathway is an evolutionarily conserved pathway that regulates organ size and maintains tissue homeostasis. Yes‑associated protein 1 (YAP1) is a key effector of this pathway and regulates downstream target genes by binding to transcriptional co‑activators with PDZ binding sequences (TAZ). Several studies have demonstrated that YAP1 is overexpressed in bladder cancer and is involved in adverse outcomes such as bladder cancer occurrence, progression, resistance to cisplatin and the recurrence of tumours. The present review summarized the involvement of YAP1 in bladder cancer disease onset and progression, and the mechanism of YAP1 involvement in bladder cancer treatment. In addition, this study further explored the potential of YAP1 in the diagnosis and treatment of bladder cancer. This study aimed to explore the potential mechanism of YAP1 in the treatment of bladder cancer.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell migration and invasion assay data in Fig. 2E and F and 4E and F, tumor images in Fig. 7B and western blotting data shown in Fig. 4D had already appeared in previously published articles written by different authors at different research institutes (a few of which have been retracted). Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 44: 1343‑1354, 2020; DOI: 10.3892/or.2020.7691].

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the immunohistochemical images shown in Fig. 7E were strikingly similar to data that had already been published in different form in a previous article in the journal PLoS One written by different authors at different research institutes. Owing to the fact that the abovementioned data had already apparently been published previously, the Editor of Oncology Reports has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 44: 1064‑1074, 2020; DOI: 10.3892/or.2020.7684].

The aberrant expression of HER family members and cancer stem cells (CSCs) have been associated with tumour progression and resistance to therapy. At present, several HER inhibitors have been approved for the treatment of patients with a range of cancers but not for the treatment of patients with hepatocellular carcinoma (HCC). The present study investigated the co‑expression and prognostic significance of HER family members, type‑III deletion mutant EGFR (EGFRvIII), and the putative CSC biomarkers CD44 and epithelial cell adhesion molecule (EpCAM) in 43 patients with HCC. The relative expression of these biomarkers was determined using immunohistochemistry. At a cut off value of >5% of tumour cells stained for these biomarkers, 35% [wild‑type (wt)EGFR], 58% (HER‑2), 0% (HER‑3), 19% (HER‑4), 26% (EGFRvIII), 40% (CD44) and 33% (EpCAM) of patients were positive. In 23, 14 and 9% of the patients, wtEGFR expression was accompanied by co‑expression with HER‑2, EGFRvIII and HER‑2/EGFRvIII, respectively. EGFRvIII expression, membranous expression of CD44 and co‑expression of wtEGFR/EGFRvIII were associated with poor overall survival (OS). By contrast, cytoplasmic CD44 expression was associated with a longer OS time. The present study also investigated the effect of several agents targeting one or more members of the HER family, other growth factor receptors and cell signalling proteins on the proliferation of HCC cell lines. Among agents targeting one or more members of the HER family, the pan‑HER family blocker afatinib was the most effective, inhibiting the proliferation of three out of seven human liver cancer cell lines (LCCLs), while the CDK inhibitor dinacicilib was the most effective agent, inhibiting the proliferation of all human LCCLs tested. Taken together, the present results suggested that EGFRvIII expression and its co‑expression with wtEGFR or CD44 was of prognostic significance. These results also support further investigations of the therapeutic potential of drugs targeting EGFRvIII and other members of the HER family in patients with HCC.

Colorectal cancer (CRC) ranks as the third most prevalent malignancy and second leading cause of cancer‑related fatalities worldwide. Immunotherapy alone or in combination with chemotherapy has a favorable survival benefit for patients with CRC. Unlike αβ T cells, which are prone to drug resistance, γδ T cells do not exhibit major histocompatibility complex restriction and can target tumor cells through diverse mechanisms. Recent research has demonstrated the widespread involvement of Vδ1T, Vδ2T, and γδ T17 cells in tumorigenesis and progression. In the present review, the influence of different factors, including immune checkpoint molecules, the tumor microenvironment and microorganisms, was summarized on the antitumor/protumor effects of these cells, aiming to provide insights for the development of more efficient and less toxic immunotherapy‑based anticancer drugs.

Cisplatin resistance is common in non‑small cell lung cancer (NSCLC); however, the molecular mechanisms remain unclear. The present study aimed to identify a new function of Golgi phosphoprotein 3 (GOLPH3) in NSCLC‑associated cisplatin resistance. Using A549 human NSCLC cells and the cisplatin‑resistant variant, stable cell lines with GOLPH3 knockdown or overexpression were established using lentiviral vectors. Through Cell Counting Kit‑8 and EdU assays, it was revealed that knockdown of GOLPH3 significantly enhanced cisplatin sensitivity in NSCLC cells. Specifically, flow cytometric analysis showed that GOLPH3 knockdown promoted apoptosis and G₂‑phase cell cycle arrest in A549 cells. Mechanistically, intracellular reactive oxygen species (ROS) and glutathione (GSH) levels were measured using assay kits, and it was demonstrated that GOLPH3 knockdown decreased intracellular GSH levels, and further attenuated intracellular cisplatin efflux and GSH/ROS imbalance. In addition, tumor‑sphere formation assays verified that GOLPH3 knockdown mitigated the stem cell‑like phenotype of NSCLC cells. In conclusion, the present findings indicated the relevance of GOLPH3 in NSCLC‑associated cisplatin resistance, and thus targeting GOLPH3 may be developed into a combination therapy to overcome cisplatin resistance.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that there appeared to be overlapping sections in a pair of the fluorescence reporter assay data panels shown in Fig. 4B; moreover, upon having conducted an independent investigation of the data in this paper in the Editorial Office, one of the data panels shown in this figure was strikingly similar to data that had previously appeared in different form in a paper written by different authors at a different research institute. Owing to the fact that the contentious data in the above article had already been published prior to its submission to Oncology Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Oncology Reports 39: 977‑984, 2018; DOI: 10.3892/or.2017.6156].

Collagen type X α1 chain (COL10A1), a gene encoding the α‑1 chain of type X collagen, serves a key role in conferring tensile strength and structural integrity to tissues. Upregulation of COL10A1 expression has been observed in different malignancies, including lung, gastric and pancreatic cancer, and is associated with poor prognosis. The present review provides an updated synthesis of the evolving biological understanding of COL10A1, with a particular focus on its mechanisms of action and regulatory functions within the context of tumorigenesis. For example, it has been established that increased COL10A1 expression promotes cancer progression by activating multiple signaling pathways, including the TGF‑β1/Smad, MEK/ERK and focal adhesion kinase signaling pathways, thereby inducing proliferation, invasion and migration. Additionally, COL10A1 has been demonstrated to induce epithelial‑mesenchymal transition and reshapes the extracellular matrix within tumor tissues. Furthermore, on the basis of methyltransferase‑like 3‑mediated N6‑methyladenosine methylation, COL10A1 intricately regulates the epitranscriptomic machinery, thereby augmenting its oncogenic role. However, although COL10A1 serves a pivotal role in gene transcription and the orchestration of tumor growth, the question of whether COL10A1 would serve as a viable therapeutic target remains a subject of scientific hypothesis requiring rigorous examination. Variables such as distinct tumor microenvironments and treatment associations necessitate further experimental validation. Therefore, a comprehensive assessment and understanding of the functional and mechanistic roles of COL10A1 in cancer may pave the way for the development of innovative cancer treatment strategies.

Renal cell carcinoma (RCC) is distinguished by its varied metabolic reprogramming driven by tumor suppressor gene dysregulation and oncogene activation. Tumors can adapt nutrient uptake and metabolism pathways to meet the altered biosynthetic, bioenergetic and redox demands of cancer cells, whereas conventional chemotherapeutics and molecular inhibitors predominantly target individual metabolic pathways without addressing this adaptability. Flavonoids, which are well‑known for their antioxidant and anti‑inflammatory properties, offer a unique approach by influencing multiple metabolic targets. The present comprehensive review reveals the intricate processes of RCC metabolic reprogramming, encompassing glycolysis, mitochondrial oxidative phosphorylation and fatty acid biosynthesis. The insights derived from the present review may contribute to the understanding of the specific anticancer mechanisms of flavonoids, potentially paving the way for the development of natural antitumor drugs focused on the metabolic reprogramming of RCC.

Cancer is one of the most prevalent diseases and the leading cause of death worldwide. Despite the improved survival rates of cancer in recent years, the current available treatments often face resistance and side effects. Drug repurposing represents a cost‑effective and efficient alternative to cancer treatment. Recent studies revealed that penfluridol (PF), an antipsychotic drug, is a promising anticancer agent. In the present study, a scoping review was conducted to ascertain the anticancer properties of PF. For this, a literature search was performed using the Scopus, PubMed and Web of Science databases with the search string 'penfluridol' AND 'cancer'. A total of 23 original articles with in vivo and/or in vitro studies on the effect of PF on cancer were included in the scoping review. The outcome of the analysis demonstrated the anticancer potential of PF. PF significantly inhibited cell proliferation, metastasis and invasion while inducing apoptosis and autophagy in vivo and across a spectrum of cancer cell lines, including breast, lung, pancreatic, glioblastoma, gallbladder, bladder, oesophageal, leukaemia and renal cancers. However, research on PF derivatives with high anticancer activities and reduced neurological side effects may be necessary.