Benzo[a]pyrene promotes progression in tongue squamous cell carcinoma

Abstract

Tongue squamous cell carcinoma (TSCC) is the most common head and neck cancer and accounts for 1%-2% of all human malignancies (Erickson, 2017). Many studies have indicated that tobacco smoking is an important risk factor for TSCC (Hashibe et al., 2009). Smoking is related to a poor prognosis in TSCC patients by decreasing survival rate and increasing the risk of recurrence, as well by increasing the incidence of secondary cancers (Warren, Kasza, Reid, Cummings, & Marshall, 2013). Smoking during cancer treatment is associated with

Effect of benzo[a]pyrene on proliferation and metastasis of oral squamous cell carcinoma cells: A transcriptome analysis based onRNA‐seq

“…In this study, we analyzed the effect of BaP on SCC‐9 cell proliferation, tumorigenicity, metastasis, invasion, and apoptosis using a CCK‐8 assay, an EdU proliferation assay, a Transwell assay, and flow cytometry, respectively. These results strongly implicated BaP promotion of OSCC cell proliferation, metastasis, invasion, and tumorigenicity, consistent with the known carcinogenic potential of BaP and findings of previous studies regarding the role of BaP in multiple types of tumors, such as hepatocellular carcinoma and lung cancer 30–32 …”

“…These results strongly implicated BaP promotion of OSCC cell proliferation, metastasis, invasion, and tumorigenicity, consistent with the known carcinogenic potential of BaP and findings of previous studies regarding the role of BaP in multiple types of tumors, such as hepatocellular carcinoma and lung cancer. 30 As shown in Figure 1, BaP promoted OSCC proliferation, but no significant difference in the promotion effect was observed among the 2, 8, and 32 μM doses of BaP, which differs from the ability of BaP to promote the migration invasion of OSCC cells in an apparent dose-dependent manner. We presumed that the optimal BaP concentration for promoting OSCC proliferation was perhaps approximately 2-8 μM; increasing drug concentrations beyond these doses did not promote proliferation more, and excessive concentrations of BaP even inhibited OSCC proliferation.…”

“…Extensive in vitro and in vivo investigations have demonstrated the capability of BaP to participate in the progression of various malignancies, including lung cancer, renal cell carcinoma, and hepatocellular carcinoma, and so forth. [29][30][31] BaP is a procarcinogenin, and upon metabolic activation in animals, it can act as a complete carcinogen and induce mutations in key genes by binding DNA, subsequently promoting tumor formation with the outgrowth of irreversibly transformed cells. 29 In this study, we analyzed the effect of BaP on SCC-9 cell proliferation, tumorigenicity, metastasis, invasion, and apoptosis using a CCK-8 assay, an EdU proliferation assay, a Transwell assay, and flow cytometry, respectively.…”

“…Extensive in vitro and in vivo investigations have demonstrated the capability of BaP to participate in the progression of various malignancies, including lung cancer, renal cell carcinoma, and hepatocellular carcinoma, and so forth 29–31 . BaP is a procarcinogenin, and upon metabolic activation in animals, it can act as a complete carcinogen and induce mutations in key genes by binding DNA, subsequently promoting tumor formation with the outgrowth of irreversibly transformed cells 29 .…”

Can Exposure to Environmental Pollutants Be Associated with Less Effective Chemotherapy in Cancer Patients?

“…In another study, squamous cell carcinoma (SCC) CAL27 and SCC9 cells treated with long-term (3 months) BaP (50 nM) showed greater chemoresistance to 5-FU (≤100 µg/mL) and CDDP (≤100 µM). Although no mechanism was analyzed to explain chemoresistance, it was mentioned that these cells also exhibited greater mobility, invasiveness, and aggressiveness, presenting shortened telomeres and diverse genomic mutations [ 18 ].…”