The prevention, diagnosis and targeted therapies of cancer are important in cancer controlling and treatment. The present challenge about cancer biomarker still remains in identifying the special biomarkers for predicting cancer risk and assessing patient's response during anticancer treatment. Lipidomics, in simple definition is the quantification of all lipids in a confined biological entity. Lipids play roles in membrane structure, energy storage, and signal transduction as well as in human cancers. Previous researches indicated that lipids may serve as a promising biomarker in the early diagnoses and individualized treatment of cancer.

The airway smooth muscle (ASM) plays an indispensable role in airway structure and function. Dysfunction in ASM plays a central role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and contributes to alterations of contractility, inflammatory response, immunoreaction, phenotype, quantity, and size of airways. ASM makes a key contribution in COPD by various mechanisms including altered contractility and relaxation induce by [Ca2+]i, cell proliferation and hypertrophy, production and modulation of extracellular cytokines, and release of pro-and-anti-inflammatory mediators. Multiple dysfunctions of ASM contribute to modulating airway responses to stimuli, remodeling, and fibrosis, as well as influence the compliance of lungs. The present review highlights regulatory roles of multiple factors in the development of ASM dysfunction in COPD, aims to understand the regulatory mechanism by which ASM dysfunctions are initiated, and explores the clinical significance of ASM on alterations of airway structure and function in COPD and development of novel therapeutic strategies for COPD.

Chronic lung diseases are highly prevalent worldwide and cause significant mortality. Lung cancer is the end stage of many chronic lung diseases. RNA epigenetics can dynamically modulate gene expression and decide cell fate. Recently, studies have confirmed that RNA epigenetics plays a crucial role in the developing of chronic lung diseases. Further exploration of the underlying mechanisms of RNA epigenetics in chronic lung diseases, including lung cancer, may lead to a better understanding of the diseases and promote the development of new biomarkers and therapeutic strategies. This article reviews basic information on RNA modifications, including N⁶ methylation of adenosine (m⁶A), N¹ methylation of adenosine (m¹A), N⁷-methylguanosine (m⁷G), 5-methylcytosine (m⁵C), 2′O-methylation (2′-O-Me or Nm), pseudouridine (5-ribosyl uracil or Ψ), and adenosine to inosine RNA editing (A-to-I editing). We then show how they relate to different types of lung disease. This paper hopes to summarize the mechanisms of RNA modification in chronic lung disease and finds a new way to develop early diagnosis and treatment of chronic lung disease.