Oncology reports最新文献

Salt‑induced kinase 1 (SIK1) is a serine/threonine protein kinase that is a member of the AMP‑activated protein kinase family. SIK is catalytically activated through its phosphorylation by the upstream kinase LKB1. SIK1 has been reported to be associated with numerous types of cancer. The present review summarizes the structure, regulatory factors and inhibitors of SIK1, and also describes how SIK1 is a signal regulatory factor that fulfills connecting roles in various signal regulatory pathways. Furthermore, the anti‑inflammatory effects of SIK1 during the early stage of tumor occurrence and its different regulatory effects following tumor occurrence, are summarized, and through collating the tumor signal regulatory mechanisms in which SIK1 participates, it has been demonstrated that SIK1 acts as a necessary node in cancer signal transduction. In conclusion, SIK1 is discussed independent of the SIKs family, its research results and recent progress in oncology are summarized in detail with a focus on SIK1, and its potential as a therapeutic target is highlighted, underscoring the need for SIK1‑targeted regulatory strategies in future cancer therapy.

Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 5A on p. 1305, the same xenograft tumor image had been selected for a pair of the GFP/U2‑OS experiments, where the images from discretely performed experiments were intended to have been shown. Furthermore, upon performing an independent analysis of the data in the Editorial Office, it was noted that the data selected for the 'SaO2/GFP/24 h' and 'SaO2/HMGN2/48 h' experiments in Fig. 4A, also on p. 1305, were strikingly similar, such that the same data had apparently been chosen to show the results of differently performed experiments. After having inspected the figures, the authors realized that one of the n=3 experimental results had inadvertently been omitted from Fig. 5A, and the data shown to represent the 'SaO2/GFP/24 h' experiment had been chosen incorrectly. The revised and corrected versions of Figs. 4 and 5 are shown on the next page (also note that erroneously written labels have been corrected in Fig. 5C: "Tumor volume" has been replaced by "Tumor weight"). Note that the errors made in terms of the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for granting them this opportunity to publish a Corrigendum, and apologize to boh the Editor and the readership for any inconvenience caused. [Oncology Reports 33: 1300‑1306, 2015; DOI: 10.3892/or.2014.3689].

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.

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 this paper, it was drawn to the Editor's attention by a concerned reader that certain of the colony formation assay data featured in Fig. 4A and C on p. 2726, tumor images in Fig. 6A on p. 2727, and western blotting data shown in Fig. 7A on p. 2728 were strikingly similar to data that had appeared in other articles written by different authors at different research institutes, which had already been published before this article was received at Oncology Reports. Owing to the fact that the abovementioned data had already been published prior to the receipt of this article at 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 34: 2722‑2730, 2015; DOI: 10.3892/or.2015.4239].

Renal cell carcinoma (RCC) is a highly aggressive neoplastic disease of the renal parenchyma that is characterized by an intrinsic resistance to cytotoxic chemotherapy; for this reason, curative treatment is only achieved through surgical intervention in its early stages. The successful treatment of advanced or metastatic RCC will require the combined use of novel targeted therapies such as tyrosine kinase inhibitors, vascular endothelial growth factor blockers and immune checkpoint blockade therapies. Unfortunately, not all patients are candidates for such treatments, and at present, it is not possible to predict a patient's therapeutic response or likelihood to develop treatment‑associated complications. The present review described the literature focusing on the use of biomarkers for predicting patients' responses to therapies that induce immune checkpoint blockade in RCC.

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.

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.