Molecular Pathology of Lung Cancer

Saller, James J.; Boyle, Theresa A.

doi:10.1101/cshperspect.a037812

Cited by 10 publications

(8 citation statements)

References 488 publications

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“…Lung cancer is the leading cause of cancer‐related death worldwide, of which NSCLC is the most common subtype. 1 , 4 The histological type and stage of lung cancer determine the treatment options and prognosis. Clinically, new biomarkers for NSCLC diagnosis and prognosis are urgently needed.…”

Section: Discussionmentioning

confidence: 99%

“…The 5‐year survival rate of lung cancer is only 10%–20% in most countries 3 . Histologically, lung cancer is divided into small cell lung cancer and non‐small cell lung cancer (NSCLC), of which the latter accounts for about 85% 4 . Thus, it is particularly urgent to identify novel diagnostic and prognostic markers for NSCLC.…”

Section: Introductionmentioning

confidence: 99%

“… 3 Histologically, lung cancer is divided into small cell lung cancer and non‐small cell lung cancer (NSCLC), of which the latter accounts for about 85%. 4 Thus, it is particularly urgent to identify novel diagnostic and prognostic markers for NSCLC. Meanwhile, the molecular mechanisms of NSCLC progression and metastasis also need to be explored to provide effective therapeutic targets for patients with metastatic disease.…”

Section: Introductionmentioning

confidence: 99%

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GPX2 promotes EMT and metastasis in non‐small cell lung cancer by activating PI3K/AKT/mTOR/Snail signaling axis

Peng

Jing

et al. 2023

FASEB BioAdvances

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Lung cancer, with non-small cell lung cancer (NSCLC) being the main subtype, is the leading cause of cancer death worldwide, which is mainly due to the cancer metastasis. Glutathione peroxidase 2 (GPX2), an antioxidant enzyme, is involved in tumor progression and metastasis. Nevertheless, the role of GPX2 in NSCLC metastasis has not been clarified. In this study, we found that GPX2 expression was elevated in NSCLC tissues and high GPX2 expression was correlated with poor prognosis in patients with NSCLC. In addtion, GPX2 expression was related to the patient's clinicopathological features, including lymph node metastasis, tumor size, and TNM stage. Overexpression of GPX2 promoted epithelial-mesenchymal transition (EMT), migration, and invasion of NSCLC cells in vitro. Knockdown of GPX2 showed the opposite effects in vitro and inhibited the metastasis of NSCLC cells in nude mice. Furthermore, GPX2 reduced reactive oxygen species (ROS) accumulation and activated the PI3K/AKT/mTOR/ Snail signaling axis. Therefore, our results indicate that GPX2 promotes EMT and metastasis of NSCLC cells by activating the PI3K/AKT/mTOR/Snail signaling axis via the removal of ROS. GPX2 may be an effective diagnostic and prognostic biomarker for NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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GPX2 promotes EMT and metastasis in non‐small cell lung cancer by activating PI3K/AKT/mTOR/Snail signaling axis

Peng

Jing

et al. 2023

FASEB BioAdvances

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“…In terms of molecular characteristics, technological advancements in recent years have allowed the identification of multiple molecular alterations in various types of tumors [ 32 ]. Among these, alterations with prognostic or therapeutic value have significantly impacted clinical practice in tumors such as lung or breast cancer, enabling personalized treatment, improving patient outcomes, and reducing the side effects associated with conventional treatment [ 33 , 34 ].…”

Section: Introductionmentioning

confidence: 99%

Molecular Classifications in Gastric Cancer: A Call for Interdisciplinary Collaboration

Díaz del Arco,

Fernández Aceñero,

Ortega Medina

2024

IJMS

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Gastric cancer (GC) is a heterogeneous disease, often diagnosed at advanced stages, with a 5-year survival rate of approximately 20%. Despite notable technological advancements in cancer research over the past decades, their impact on GC management and outcomes has been limited. Numerous molecular alterations have been identified in GC, leading to various molecular classifications, such as those developed by The Cancer Genome Atlas (TCGA) and the Asian Cancer Research Group (ACRG). Other authors have proposed alternative perspectives, including immune, proteomic, or epigenetic-based classifications. However, molecular stratification has not yet transitioned into clinical practice for GC, and little attention has been paid to alternative molecular classifications. In this review, we explore diverse molecular classifications in GC from a practical point of view, emphasizing their relationships with clinicopathological factors, prognosis, and therapeutic approaches. We have focused on classifications beyond those of TCGA and the ACRG, which have been less extensively reviewed previously. Additionally, we discuss the challenges that must be overcome to ensure their impact on patient treatment and prognosis. This review aims to serve as a practical framework to understand the molecular landscape of GC, facilitate the development of consensus molecular categories, and guide the design of innovative molecular studies in the field.

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“…Lung cancer is one of the leading causes of cancer-related death worldwide. Despite great advances in novel treatments over the past few decades, the survival rate is still low compared to that of other cancers ( 1 , 2 ). Non-small cell lung cancer (NSCLC) is the most common form, accounting for 85% of new diagnoses of lung cancer ( 3 , 4 ).…”

Section: Introductionmentioning

confidence: 99%

HS‑1793 inhibits cell proliferation in lung cancer by interfering with the interaction between p53 and MDM2

et al. 2022

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The transcription factor or tumor suppressor protein p53 regulates numerous cellular functions, including cell proliferation, invasion, migration, senescence and apoptosis, in various types of cancer. HS-1793 is an analog of resveratrol, which exhibits anti-cancer effects on various types of cancer, including breast, prostate, colon and renal cancer, and multiple myeloma. However, to the best of our knowledge, the role of HS-1793 in lung cancer remains to be examined. The present study aimed to investigate the anti-cancer effect of HS-1793 on lung cancer and to determine its association with p53. The results revealed that HS-1793 reduced cell proliferation in lung cancer and increased p53 stability, thereby elevating the expression levels of the target genes p21 and mouse double minute 2 homolog (MDM2). When the levels of MDM2, a negative regulator of p53, are increased under normal conditions, MDM2 binds and degrades p53; however, HS-1793 inhibited this binding, confirming that p53 protein stability was increased. In conclusion, the findings of the present study provide new evidence that HS-1793 may inhibit lung cancer proliferation by disrupting the p53-MDM2 interaction.

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Molecular Pathology of Lung Cancer

Cited by 10 publications

References 488 publications

GPX2 promotes EMT and metastasis in non‐small cell lung cancer by activating PI3K/AKT/mTOR/Snail signaling axis

GPX2 promotes EMT and metastasis in non‐small cell lung cancer by activating PI3K/AKT/mTOR/Snail signaling axis

Molecular Classifications in Gastric Cancer: A Call for Interdisciplinary Collaboration

HS‑1793 inhibits cell proliferation in lung cancer by interfering with the interaction between p53 and MDM2

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