Autophagy analysis in oral carcinogenesis

Lima, Taiane Berguermaier de; Paz, Ana Helena da Rosa; Rados, Pantelis Varvaki; Leonardi, Rosalia; Bufo, Pantaleo; Pedicillo, Maria Carmela; Santoro, Angela; Cagiano, Simona; Aquino, Gabriella; Botti, Gerardo; Pannone, Giuseppe; Visioli, Fernanda

doi:10.1016/j.prp.2017.07.027

Cited by 8 publications

(5 citation statements)

References 29 publications

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“…Liu et al have found that the expression of LC3-II and Beclin-1/BECN1 were upregulated in leuk-1 cells upon CS stimulation and this upregulation was in a concentration- and time-dependent manner [ 78 ], suggesting that CS exposure could trigger the autophagy of human oral epithelial cells. Similarly, Lima et al also confirmed the significant elevation in the percentage of LC3-II positive cells from the normal oral mucosa to the leukoplakia samples, especially in the upper layers of the epithelium [ 79 ]. Interestingly, the aberrant expression of lncRNAs was also found in OLK.…”

Section: The Evs-borne Cargo Are Changed By Cs Exposurementioning

confidence: 81%

“…To be specific, the classical autophagy-related proteins LC3-II and Beclin-1 were upregulated in a concentration- and time-dependent manner [ 78 ]. As we mentioned above, the LC3-II was also overexpressed in the leukoplakia samples, especially in the upper layers of the epithelium, compared to the normal tissues [ 79 ]. Based on the data, we infer that the alteration of CSE-induced EVs might upregulate the autophagy of oral mucosal epithelial cells by upregulating LC3-II and Beclin-1, and ultimately contributes to the progression of OLK.…”

Section: Cs-induced Evs As Mediators For Intra/inter-cellular Message...mentioning

confidence: 99%

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The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia

et al. 2023

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Background The onset of oral leukoplakia (OLK), the most common oral lesion with a high risk of malignant transformation, is closely associated with the exposure of cigarette smoke. Cigarette smoke is a complicated mixture of more than 4500 different chemicals including various oxidants and free radical, which contributes to the onset of immune and inflammatory response or even carcinogenesis. Recent studies have proved that the exposure of cigarette smoke leads to the onset and aggravation of many diseases via significantly changed the production and components of extracellular vesicles. The extracellular vesicles are membrane-enclosed nanosized particles secreted by diverse cells and involved in cell–cell communication because of their ability to deliver a number of bioactive molecules including proteins, lipids, DNAs and RNAs. Getting insight into the mechanisms of extracellular vesicles in regulating OLK upon cigarette smoke stimulation contributes to unravel the pathophysiology of OLK in-depth. However, evidence done on the role of extracellular vesicles in cigarette smoke-induced OLK is still in its infancy. Materials and methods Relevant literatures on cigarette smoke, oral leukoplakia and extracellular vesicles were searched in PubMed database. Conclusions In this review, we summarize the recent findings about the function of extracellular vesicles in the pathogenesis of cigarette smoke-induced diseases, and to infer their potential utilizations as diagnostic biomarkers, prognostic evaluation, and therapeutic targets of OLK in the future.

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Section: The Evs-borne Cargo Are Changed By Cs Exposurementioning

confidence: 81%

Section: Cs-induced Evs As Mediators For Intra/inter-cellular Message...mentioning

confidence: 99%

The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia

et al. 2023

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“…LC3 is a specific marker of autophagosomes [32]. When autophagy occurs, the cytoplasmic form LC3-I binds to phospholipid amines through an ubiquitin-like enzyme reaction, converts it to the phospholipid-conjugated form LC3-II, and is continuously recruited into autophagic vacuoles to initiate the autophagy process [33,34]. Autophagyrelated signal transduction pathways are complex and interact with each other.…”

Section: Discussionmentioning

confidence: 99%

Extracorporeal shock wave protects chondrocytes against interleukin-1β-induced apoptosis and promotes autophagy in vitro

Wang¹,

Tang²,

Min³

2023

ScienceAsia

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Osteoarthritis (OA) is a common joint disease, but there is no effective treatment except surgery at present. Extracorporeal shock wave (ESW) is an emerging therapy widely used in various medical fields. In this study, we mainly investigated the effects of ESW on apoptosis and autophagy of osteoarthritic chondrocytes by analyzing the cell apoptosis and the expression of autophagy markers' mRNAs and proteins, respectively. Primary chondrocytes were isolated from articular cartilage tissue of rats. Results showed that ESW effectively inhibited the interleukin-1β-induced (IL-1β-induced) chondrocyte apoptosis. Moreover, ESW treatment elevated the mRNA and the protein expression levels of Beclin 1, Atg5, LC3B, and Collagen II. Beclin 1 plays a key role in autophagy, positively regulating autophagic activity. Atg5 is a marker of autophagic activity, and LC3 is a specific marker of autophagosome. Collagen II is an important indicator to judge the functional activity of chondrocytes. In contrast, the mRNA and the protein expression levels of P62, which is a measure of autophagic flux and is thought to be negatively correlated with autophagic degradation, were decreased in the ESW treated cells. This study reveals the role of ESW in promoting chondrocyte autophagy and suppressing cell apoptosis. Thus, ESW may protect chondrocytes against IL-1β-induced apoptosis and promote autophagy in an in vitro model of osteoarthritis.

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“…A recent study has shown that oxaliplatin-induced protective autophagy could partially antagonize apoptosis in gastric cancer MGC803 cells, promoting tumor progression ( Xu et al, 2011 ). The expression levels of LC3II have been reported to be positively correlated with the clinical stages in oral squamous carcinoma (OSCC) ( de Lima et al, 2017 ). Some normal cells contribute to tumor cell growth by generating nutritional autophagy at the early stage of tumor development ( Maes et al, 2013 ; Katheder et al, 2017 ).…”

Section: The Role Of Autophagy In Tumorigenesismentioning

confidence: 99%

Microorganism-regulated autophagy in gastrointestinal cancer

Xu,

Fan,

et al. 2023

PeerJ

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Gastrointestinal cancer has always been one of the most urgent problems to be solved, and it has become a major global health issue. Microorganisms in the gastrointestinal tract regulate normal physiological and pathological processes. Accumulating evidence reveals the role of the imbalance in the microbial community during tumorigenesis. Autophagy is an important intracellular homeostatic process, where defective proteins and organelles are degraded and recycled under stress. Autophagy plays a dual role in tumors as both tumor suppressor and tumor promoter. Many studies have shown that autophagy plays an important role in response to microbial infection. Here, we provide an overview on the regulation of the autophagy signaling pathway by microorganisms in gastrointestinal cancer.

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Autophagy analysis in oral carcinogenesis

Cited by 8 publications

References 29 publications

The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia

The potential roles of cigarette smoke-induced extracellular vesicles in oral leukoplakia

Extracorporeal shock wave protects chondrocytes against interleukin-1β-induced apoptosis and promotes autophagy in vitro

Microorganism-regulated autophagy in gastrointestinal cancer

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