Metastasis is the main cause of cancer-related mortality. Although the actual process of metastasis remains largely elusive, epithelial-mesenchymal transition (EMT) has been considered as a major event in metastasis. Besides, hypoxia is common in solid cancers and has been considered as an important factor for adverse treatment outcomes including metastasis. Since EMT and hypoxia potentially share several signaling pathways, many recent studies focused on investigate the issue of hypoxia-induced EMT. Among all potential mediators of hypoxia-induced EMT, hypoxia-inducible factor-1α (HIF-1α) has been studied extensively. Moreover, there are other potential mediators that may also contribute to the process. This review aims to summarize the recent reports on hypoxia-induced EMT by HIF-1α or other potential mediators and provide insights for further investigations on this issue. Ultimately, better understanding of hypoxia-induced EMT may allow us to develop anti-metastatic strategies and improve treatment outcomes.

Photobiomodulation (PBM) using low-level laser therapy (LLLT) is a treatment that is increasingly used in oncology. Studies reported enhancement of wound healing with reduction in pain, tissue swelling and inflammatory conditions such as radiation dermatitis, oral mucositis, and lymphedema. However, factors such as wavelength, energy density and irradiation frequency influence the cellular mechanisms of LLLT. Moreover, the effects of LLLT vary according to cell types. Thus, controversy arose as a result of poor clinical response reported in some studies that may have used inadequately planned treatment protocols. Since LLLT may enhance tumor cell proliferation, these will also need to be considered before clinical use. This review aims to summarize the current knowledge of the cellular mechanisms of LLLT by considering its effects on cell proliferation, metabolism, angiogenesis, apoptosis and inflammation. With a better understanding of the cellular mechanisms, bridging findings from laboratory studies to clinical application can be improved.

Autophagy is an important catabolic process in which cells digest and recycle their own cytoplasmic contents for maintaining cellular homeostasis. Interestingly, autophagy could play both pro-death and pro-survival roles in influencing the development of cancer via various signal pathways. As radiotherapy is one of the main treatment modalities for cancer, we reviewed the effect of autophagy modulations on radiosensitivity and radiotherapy efficacy in various cancer types. The future development of autophagy modifications for improving radiotherapy efficacy and cancer prognosis will also be discussed.

Background and Objective: Lung cancer remains the leading cause of cancer-related mortality worldwide, with a 5-year survival rate ranging from 10% to 20%. The majority of cases are categorized as non-small cell lung cancer (NSCLC) (80%) and small cell lung cancer (SCLC) (20%), with NSCLC being the more prevalent type. Tobacco use, particularly cigarette smoking, is a significant contributor to over 80% of lung cancer cases. Early diagnosis is challenging due to limitations in screening methods, resulting in many cases being identified only in advanced stages. Moreover, current treatment options often exhibit low efficacy, partly due to an inadequate understanding of the disease’s pathogenesis. This narrative review aims to summarize recent discoveries and advancements in lung cancer research, focusing on improvements in diagnosis, treatment, and understanding of the disease. Methods: A comprehensive literature review was performed utilizing the PubMed Central database to identify recent studies relevant to lung cancer. This review synthesizes findings from various research articles to provide a cohesive summary of advancements in the field. Key Content and Findings: In the past decade, notable progress has been achieved in lung cancer research, particularly concerning diagnostics and treatment strategies. Novel therapeutic approaches, including immunotherapy and genomic-targeted therapies, have demonstrated promising results. Understanding the tumor microenvironment (TME) and the role of T lymphocytes has become crucial for developing effective treatments. Additionally, advancements in immune checkpoint inhibitors (ICIs) have shown potential in enhancing patient outcomes. Improvements in tumor detection technologies are also anticipated to facilitate earlier diagnosis, ultimately contributing to better survival rates. Conclusions: Significant strides have been made in lung cancer research over the last ten years, particularly in diagnostics and treatment methodologies. Future research should prioritize exploring the TME, the function of T lymphocytes, and the efficacy of ICIs while continuing to innovate in tumor detection technologies. Such efforts are essential for enhancing treatment outcomes and improving the overall quality of life for lung cancer patients.

The c-Jun N-terminal kinases (JNKs) are a group of mitogen-activated protein kinases (MAPKs). JNK is mainly activated under stressful conditions or by inflammatory cytokines and has multiple downstream targets for mediating cell proliferation, differentiation, survival, apoptosis, and immune responses. JNK has been demonstrated to have both tumor promoting and tumor suppressing roles in different cancers depending on the focused pathway in each study. JNK also plays complex roles in the heterogeneous tumor microenvironment (TME). JNK is involved in different tumorigenesis pathways. TME closely relates with tumor development and consists of various stressful and chronic inflammatory conditions along with different cell populations, in which the JNK pathway may have various mediating roles. In this review, we aim to summarize the present knowledge of JNK-mediated processes in TME, including hypoxia, reactive oxygen species, inflammation, immune responses, angiogenesis, as well as the regulation of various cell populations within TME. This review also suggests future research directions for translating JNK modulation in pre-clinical findings to clinical benefits.