Environmental heavy metal as a potential risk factor for the progression of oral potentially malignant disorders in central Taiwan

Tsai, Kuo-Yang; Su, Chin-Chuan; Chiang, Chi Ting; Tseng, Yao Ting; Lian, Ie Bin

doi:10.1016/j.canep.2017.02.003

Cited by 30 publications

(29 citation statements)

References 28 publications

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“…The death rate of oral cancer was 11.4 per 100, 000 population [1, 2]. In Taiwan, the major risk factors of oral cancer are betel nut chewing [3–6], smoking [7], alcohol consumption [4, 8], inflammation [9, 10] and human papilloma virus (HPV) infection [11, 12]. The 5-year survival rate of oral cancer is 50% [13, 14].…”

Section: Introductionmentioning

confidence: 99%

YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

Lee¹,

Lin²,

Lu³

et al. 2017

BioMedicine

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Oral cancer is a serious and fatal disease. Cisplatin is the first line of chemotherapeutic agent for oral cancer therapy. However, the development of drug resistance and severe side effects cause tremendous problems clinically. In this study, we investigated the pharmacologic mechanisms of YC-1 on cisplatin-resistant human oral cancer cell line, CAR. Our results indicated that YC-1 induced a concentration-dependent and time-dependent decrease in viability of CAR cells analyzed by MTT assay. Real-time image analysis of CAR cells by IncuCyte™ Kinetic Live Cell Imaging System demonstrated that YC-1 inhibited cell proliferation and reduced cell confluence in a time-dependent manner. Results from flow cytometric analysis revealed that YC-1 promoted G0/G1 phase arrest and provoked apoptosis in CAR cells. The effects of cell cycle arrest by YC-1 were further supported by up-regulation of p21 and down-regulation of cyclin A, D, E and CDK2 protein levels. TUNEL staining showed that YC-1 caused DNA fragmentation, a late stage feature of apoptosis. In addition, YC-1 increased the activities of caspase-9 and caspase-3, disrupted the mitochondrial membrane potential (AYm) and stimulated ROS production in CAR cells. The protein levels of cytochrome c, Bax and Bak were elevated while Bcl-2 protein expression was attenuated in YC-1-treated CAR cells. In summary, YC-1 suppressed the viability of cisplatin-resistant CAR cells through inhibiting cell proliferation, arresting cell cycle at G0/G1 phase and triggering mitochondria-mediated apoptosis. Our results provide evidences to support the potentially therapeutic application of YC-1 on fighting against drug resistant oral cancer in the future.

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Section: Introductionmentioning

confidence: 99%

YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

Lee¹,

Lin²,

Lu³

et al. 2017

BioMedicine

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“…Tobacco smoking and alcohol consumption are also key risk factors for oral cancer in Taiwan. Smokers have a higher risk of potentially malignant oral disorders (hazard ratio of 2.8) than nonsmokers [12]. ADH1B, one of the genes encoding the ADH enzyme, and ALDH2, a gene that encodes an enzyme responsible for the conversion of acetaldehyde to acetate, may be associated with head and neck cancer in alcohol drinkers [13].…”

Section: Introductionmentioning

confidence: 99%

Role and Mechanism of LIF in Oral Squamous Cell Carcinoma Progression

Lin

et al. 2020

JCM

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Background: Metastasis is a severe problem in patients with oral squamous cell carcinoma (OSCC), which is the fifth most common cancer worldwide. Leukemia inhibitory factor (LIF) has been studied in different cancers, while the role of LIF in OSCC remains unclear. Methods: LIF expression was detected in 100 OSCC samples by immunohistochemistry. Effects of LIF on cell motility were evaluated in OSCC cell lines. High-throughput microarray analysis was also conducted. The correlation between LIF and the downstream effector was analyzed by real-time quantitative reverse transcription PCR. Results: Patients with OSCC who had lymph node metastasis or advanced cancer stages showed high LIF expression. OSCC patients with higher LIF expression, advanced stage, large tumor size, or lymph node metastasis had significantly shorter overall survival. LIF regulated cancer cell motilities through outside-in signaling. The inhibin beta A subunit (INHBA) gene was identified as a crucial downstream effector of LIF-promoted OSCC progression and restored migration and invasion abilities in LIF knockdown transfectants. Conclusion: LIF enhances regional lymphatic spread, thus leading to an advanced cancer stage. Regulation of LIF downstream molecules such as INHBA inhibits the invasion or migration ability of cancer cells. Thus, LIF can be a potential target in preventing cancer metastasis and spread.

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“…To the present time, more than 7000 chemical substances have been identified in cigarette smoke, including aromatic hydrocarbons, aldehydes, ketones, and heavy metals (Condoluci et al 2016;Stewart and Wild 2014). Although some metals are considered essential for biological functions, balance, high exposure to lead (Pb), cadmium (Cd), arsenic (As), nickel (Ni), and chromium (Cr), which are present in soil, contaminating food, and tobacco smoke, are also considered risk factors for cancer (Condoluci et al 2016;Galazyn-Sidorczuk et al 2008;Koedrith et al 2013;Maret 2016;Tsai et al 2017;Viana et al 2011). From the contamination of soil, tobacco leaves can be exposed to the metals: lead (Pb), cadmium (Cd), arsenic (As), nickel (Ni), and chromium (Cr), copper (Cu), and zinc (Zn), but its concentrations are dependent on plant growth and soil pH (the lower soil pH, the higher the metal contamination capacity) (Golia et al 2009).…”

Section: Introductionmentioning

confidence: 99%

“…Some carcinogens as physical, chemical, or viral agents are well known, but heavy metal's relation to malignant neoplasms and the mechanism by which it induces carcinogenesis remain unclear (Condoluci et al 2016;Galazyn-Sidorczuk et al 2008;Koedrith et al 2013;Maret 2016;Tsai et al 2017;Viana et al 2011;Wise et al 2017). Metals such as cadmium, arsenic, nickel, and chromium are already classified as carcinogenic to humans (Groups 1 and 2) by the International Agency for Research on Cancer (WHO-IARC.…”

Section: Introductionmentioning

confidence: 99%

“…Chronic exposures to low concentrations of arsenic were associated with diseases such as hepatic fibrosis, cirrhosis, hepatocellular carcinoma, melanosis, hyperkeratosis, diabetes mellitus, immunological disorders, pulmonary infections, hypertension, and cardiovascular and neuromuscular diseases (Ahmed et al 2013). Similarly, exposure to high environmental nickel levels was related to an increased risk of oral carcinoma and premalignant lesion development (Tsai et al 2017).…”

Section: Introductionmentioning

confidence: 99%

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Tobacco influence in heavy metals levels in head and neck cancer cases

Bandeira

Almeida

Carta

et al. 2018

Environ Sci Pollut Res

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Heavy metals intoxication is known to be risk factors for various diseases, including cancer. These metals may be presented in food and soil as well as in leaf and tobacco smoke. The aim of this study was to correlate the exposure to heavy metals stemming from tobacco and head and neck squamous cell carcinoma carcinogenesis. Analysis of lead, copper, manganese, arsenic, chromium, and cadmium by atomic absorption spectrophotometry was performed in whole blood samples from 91 patients: 68 smokers with oral cavity, pharynx, or laryngeal cancer; 8 non-smokers with oral or larynx cancer; and 15 non-cancer smokers with tobacco-related diseases (control group). No differences were found in metals quantifications, except a significant difference was observed (p = 0.0223) with higher mean in copper levels for non-smokers with cancer. The present study concluded, for the groups evaluated, it was not possible to prove the relationship between the studied metals in the development of the neoplasm. On the other hand, the results of copper demonstrated a correlation with smokers with cancer and lower levels of circulating copper.

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Environmental heavy metal as a potential risk factor for the progression of oral potentially malignant disorders in central Taiwan

Cited by 30 publications

References 28 publications

YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

Role and Mechanism of LIF in Oral Squamous Cell Carcinoma Progression

Tobacco influence in heavy metals levels in head and neck cancer cases

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Environmental heavy metal as a potential risk factor for the progression of oral potentially malignant disorders in central Taiwan

Cited by 30 publications

References 28 publications

YC-1 induces G0/G1phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

YC-1 induces G0/G1phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

Role and Mechanism of LIF in Oral Squamous Cell Carcinoma Progression

Tobacco influence in heavy metals levels in head and neck cancer cases

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YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells

YC-1 induces G₀/G₁phase arrest and mitochondria-dependent apoptosis in cisplatin-resistant human oral cancer CAR cells