Oncology reports最新文献

Ursolic acid (UA), a pentacyclic triterpenoid that has been found in a broad variety of fruits, spices and medicinal plants, has various biological effects such as reducing inflammation, protecting cells from damage, and preserving brain function. However, its impact on ferroptosis in cancer stem‑like cells remains unexplored. The present study investigated the effect of UA on MDA‑MB‑231 and BT‑549 cell‑derived triple‑negative breast CSCs (BCSCs) and its potential ferroptosis pathway. The effects of ferroptosis on BCSCs were demonstrated by the detection of ferroptosis‑related indexes including the intracellular level of glutathione, malondialdehyde, reactive oxygen species and iron. The effects of UA on the biological behaviors of BCSCs were analyzed by Cell Counting Kit‑8, stemness indexes detection and mammosphere formation assay. The mechanism of UA induction on BCSCs was explored by reverse transcription‑quantitative PCR and western blotting. BALB/c‑nude mice were subcutaneously injected with MDA‑MB‑231‑derived BCSCs to establish xenograft models to detect the effects of UA in vivo. The results revealed that BCSCs have abnormal iron metabolism and are less susceptible to ferroptosis. UA effectively reduces the stemness traits and proliferation of BCSCs in spheroids and mice models by promoting ferroptosis. It was observed that UA stabilizes Kelch‑like ECH‑associated protein 1 and suppresses nuclear factor erythroid‑related factor 2 (NRF2) activation. These findings suggested that the ability of UA to trigger ferroptosis through the inhibition of the NRF2 pathway could be a promising approach for treating BCSCs, potentially addressing metastasis and drug resistance in triple‑negative breast cancer (TNBC). This expands the clinical applications of UA and provides a theoretical basis for its use in TNBC treatment.

Breast cancer, a prominent cause of mortality among women, develops from abnormal growth of breast tissue, thereby rendering it one of the most commonly detected cancers in the female population. Although numerous treatment strategies are available for breast cancer, discordance in terms of effective treatment and response still exists. Recently, the potential of signaling pathways and transcription factors has gained substantial attention in the cancer community; therefore, understanding their role will assist researchers in comprehending the onset and advancement of breast cancer. Forkhead box (FOX) proteins, which are important transcription factors, are considered crucial regulators of various cellular activities, including cell division and proliferation. The present study explored several subclasses of FOX proteins and their possible role in breast carcinogenesis, followed by the interaction between microRNA (miRNA) and FOX proteins. This interaction is implicated in promoting cell infiltration into surrounding tissues, ultimately leading to metastasis. The various roles that FOX proteins play in breast cancer development, their intricate relationships with miRNA, and their involvement in therapeutic resistance highlight the complexity of breast cancer dynamics. Therefore, recognizing the progress and challenges in current treatments is crucial because, despite advancements, persistent disparities in treatment effectiveness underscore the need for ongoing research, with future studies emphasizing the necessity for targeted strategies that account for the multifaceted aspects of breast cancer.

Immunotherapy, particularly immune checkpoint inhibitors (ICIs), is undoubtedly one of the major breakthroughs in lung cancer research. Patient survival and prognosis have all been improved as a result, although numerous patients do not respond to immunotherapy due to various immune escape mechanisms of the tumor cells. Recent preclinical and clinical evidence has shown that stereotactic body radiotherapy (SBRT), also known as stereotactic ablative radiotherapy, has a prominent immune priming effect that could elicit antitumor immunity against specific tumor antigens and destroy distant tumor cells, thereby achieving the elusive abscopal effect, with the resulting immuno‑active tumor environment also being more conducive to ICIs. Some landmark trials have already demonstrated the survival benefit of the dynamic duo of SBRT plus immunotherapy in metastatic non‑small‑cell lung cancer, while others such as PEMBRO‑RT further suggest that the addition of SBRT to immunotherapy could expand the current indication to those who have historically responded poorly to ICIs. In the present review, the biological mechanisms that drive the synergistic effect of SBRT and immunotherapy were first briefly outlined; then, the current understanding from clinical trials was summarized and new insight into the evolving role of immunotherapy and SBRT synergy in lung cancer treatment was provided. Finally, novel avenues for discovery were highlighted. The innovation of the present review lies in the inclusion of non‑ICI immunotherapy in the discussion, which provides a more comprehensive view on the current development and future trend of SBRT + immunotherapy synergy.

Diffuse large B‑cell lymphoma (DLBCL) is the most common pathological type of non‑Hodgkin's lymphoma. Although the development of monoclonal antibodies, small‑molecule‑targeted drugs and novel chemotherapeutic agents, and the increased use of immunotherapy have markedly improved the outcomes of DLBCL, ~40% of patients cannot be cured following the use of standardized first‑line treatment. In addition, the specific mechanisms of drug resistance and potential factors associated with a poor prognosis in these patients remain unclear. Proteomics research is used to determine potential associations between changes in DLBCL protein expression levels and different stages of disease occurrence and development. Proteomics may aid in the identification of novel molecular mechanisms and drug resistance mechanisms, through identifying multiple associated proteins and monitoring changes in expression levels. Thus, proteomics research may exhibit potential in the development of therapeutic targets and in improving prognostic evaluation in patients with DLBCL. The present study aimed to review the use of proteomic methods for the investigation of DLBCL, including the mechanisms underlying disease progression and drug resistance in DLBCL, and the function of the tumor microenvironment in lymphoma growth. The present review also demonstrated the potential of proteomic‑guided therapeutic strategies for DLBCL and discussed the synergistic benefits of using proteomic methods in DLBCL research.

Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Transwell cell migration and invasion assay data featured in Figs. 5C and 6C were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to Oncology Reports, or were submitted for consideration for publication at around the same time. In view of the fact that certain of these data had already apparently been published prior to the submission of this article for publication, 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 37: 2743‑2750, 2017; DOI: 10.3892/or.2017.5555].

Prostate cancer (PCa) affects males of all racial and ethnic groups, and leads to higher rates of mortality in those belonging to a lower socioeconomic status due to the late detection of the disease. PCa affects middle‑aged males between the ages of 45 and 60 years, and is the highest cause of cancer‑associated mortality in Western countries. As the most abundant and common mRNA modification in higher eukaryotes, N⁶‑methyladenosine (m⁶A) is widely distributed in mammalian cells and influences various aspects of mRNA metabolism. Recent studies have found that abnormal expression levels of various m⁶A regulators significantly affect the development and progression of various types of cancer, including PCa. The present review discusses the influence of m⁶A regulatory factors on the pathogenesis and progression of PCa through mRNA modification based on the current state of research on m⁶A methylation modification in PCa. It is considered that the treatment of PCa with micro‑molecular drugs that target the epigenetics of the m⁶A regulator to correct abnormal m⁶A modifications is a direction for future research into current diagnostic and therapeutic approaches for PCa.

Definitive concurrent chemoradiotherapy has been the main standard treatment method for unresectable locally advanced esophageal squamous cell cancer (ESCC) since 1999. However, several disadvantages continue to be associated with this type of treatment, including a high local failure rate (reaching ~50% within 3 years) and a median overall survival (OS) time of 16.9 months. In addition, the 5‑year overall survival rate of patients remains relatively low, at only ~21% for patients with ESCC with TNM stage T1‑3N0‑1M0. Burgeoning clinical trials and continually updating treatment modalities are currently in the process of being developed for the treatment of unresectable locally advanced ESCC. Compared with definitive concurrent chemoradiotherapy alone, clinical trials that have examined the efficacy of induction therapy, consolidation therapy, immunotherapy and targeted therapy have observed a prolonged median progression‑free survival and OS. Salvage surgery can also bring benefits to some patients. Therefore, the present review aimed to provide a comprehensive overview on the latest progress that is being made in the development of treatment strategies for unresectable locally advanced ESCC, taking into account the several new challenges that need to be overcome.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the Transwell cell invasion and migration assay data shown in Figs. 2C and 5D were strikingly similar to data in different form in other articles written by different authors at different research institutes, which had either already been published or had been submitted for publication at around the same time (some of which have now been retracted). Owing to the fact that certain of the 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 36: 2329‑2338, 2016; DOI: 10.3892/or.2016.5007].

Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 1E on p. 1885, the STAT3 blots shown for the A549 and A2780 cell lines were strikingly similar, such that these data were possibly derived from the same original source where the panels were intended to show the results from differently performed experiments. Upon examining their original data, the authors have realized that an inadvertent error was made in assembling the data in the figure, and the STAT3 data shown correctly for the A549 cell line were erroneously copied across for the A2780 cell line. The corrected version of Fig. 1, showing the correct STAT3 blot for the A2780 cell line in Fig. 1E, is shown on the next page. Note that this error did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [Oncology Reports 39: 1883‑1891, 2018; DOI: 10.3892/or.2018.6232].

Melanoma is the most lethal type of skin cancer with an increasing cutaneous cancer‑related mortality rate worldwide. Despite therapeutic advances in targeted therapy and immunotherapy, the overall survival of patients with melanoma remains unsatisfactory. Thus, a further understanding of the pathogenesis of melanoma may aid towards the development of therapeutic strategies. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) is a key enzyme that converts lysophosphatidylcholine into phosphatidylcholine in lipid remodeling. In the present study, LPCAT1 was found to play a pro‑proliferative role in melanoma. Firstly, the expression of LPCAT1 was found to be upregulated in tissues from patients with melanoma compared with that in benign nevi. Subsequently, LPCAT1 knockdown was performed, utilizing short hairpin RNA, which induced melanoma cell cycle arrest at the G1/S transition and promoted cell death. Moreover, LPCAT1 facilitated melanoma cell growth in an Akt‑dependent manner. In summary, the results of the present study indicate that targeting LPCAT1 may impede cell proliferation by inhibiting Akt signaling, thus providing a promising therapeutic strategy for melanoma in clinical practice.