Residential proximity to industrial pollution sources and colorectal cancer risk: A multicase-control study (MCC-Spain)

García‐Pérez, Javier; Larrea-Baz, Nerea Fernández de; Lope, Virginia; Molina, A.; O’Callaghan-Gordo, Cristina; Alonso, M. Henar; Rodríguez-Suárez, Marta María; Mirón-Pozo, Benito; Alguacil, Juan; Gómez‐Acebo, Inés; Ascunce, Nieves; Vanaclocha-Espí, Mercedes; Amiano, Pilar; Chirlaque, María Dolores; Simó, Vicente; Jiménez-Moleón, José Juan; Tardón, Adonina; Moreno, Vı́ctor; Castaño‐Vinyals, Gemma; Martín, Vicente; Aragonés, Núria; Pérez‐Gómez, Beatriz; Kogevinas, Manolis; Pollán, Marina

doi:10.1016/j.envint.2020.106055

Cited by 35 publications

(18 citation statements)

References 45 publications

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“…Recently, the relationship between NP exposure and incidence of CRC has been considered. A Spanish study also found a high risk of CRC in people living near industries releasing NP (Garcia-Perez et al, 2020). Because NP was wildly found in the environment and could be stored in human tissues, people in non-industrial areas may also be exposed to large amounts of NP.…”

Section: Discussionmentioning

confidence: 97%

“…Recently, the relationship between NP exposure and risk of CRC progression has been a concern. The risk of CRC has significantly increased in populations living near the industries, which release NP, in Spain (Garcia-Perez et al, 2020). Our previous studies have revealed that NP promoted CRC cell proliferation (Xie et al, 2019;Yang et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2

Wang

Zhang

et al. 2021

Front. Cell Dev. Biol.

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Recently, the effect of endocrine-disrupting chemicals on the cancer procession has been a concern. Nonylphenol (NP) is a common environmental estrogen that has been shown to enhance the proliferation of colorectal cancer (CRC) cells in our previous studies; however, the underlying mechanism remains unclear. In this study, we confirmed the increased concentration of NP in the serum of patients with CRC. RNA sequencing was used to explore the differentially expressed genes after NP exposure. We found 16 upregulated genes and 12 downregulated genes in COLO205 cells after NP treatment. Among these differentially expressed genes, we found that coiled-coil domain containing 80 (CCDC80) was downregulated by NP treatment and was associated with CRC progression. Further experiments revealed that the overexpression of CCDC80 significantly suppressed NP-induced cell proliferation and recovered the reduced cell apoptosis. Meanwhile, the overexpression of CCDC80 significantly inhibited the activation of ERK1/2 induced by NP treatment. ERK1/2 inhibitor (PD98059) treatment also suppressed NP-induced CRC cell growth, but the overexpression of CCDC80 did not enhance the effect of ERK1/2 inhibitor. Taken together, NP treatment significantly inhibited the expression of CCDC80, and the overexpression of CCDC80 suppressed NP-induced CRC cell growth by inhibiting the activation of ERK1/2. These results suggest that NP could induce CRC cell growth by influencing the expression of multiple genes. CCDC80 and ERK1/2 inhibitors may be suitable therapeutic targets in NP-related CRC progression.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2

Wang

Zhang

et al. 2021

Front. Cell Dev. Biol.

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“…In particular, if they are far in the graph, we will take advantage of this to place them far in the embedding (proportionally). For example, these entities may cause pollution, radiation or heat [8,30]. Alternatively, in the case of utilities, we may want to cover as large area as we can.…”

Section: Definition 27 (K × R Distance Approximation Parameter)mentioning

confidence: 99%

Grid Recognition: Classical and Parameterized Computational Perspectives

Gupta¹,

Sa'ar²,

Zehavi³

2021

Preprint

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Grid graphs, and, more generally, k × r grid graphs, form one of the most basic classes of geometric graphs. Over the past few decades, a large body of works studied the (in)tractability of various computational problems on grid graphs, which often yield substantially faster algorithms than general graphs. Unfortunately, the recognition of a grid graph (given a graph G, decide whether it is a grid graph) is particularly hard-it was shown to be NP-hard even on trees of pathwidth 3 already in 1987. Yet, in this paper, we provide several positive results in this regard in the framework of parameterized complexity (additionally, we present new and complementary hardness results). Specifically, our contribution is threefold. First, we show that the problem is fixed-parameter tractable (FPT) parameterized by k + mcc where mcc is the maximum size of a connected component of G. This also implies that the problem is FPT parameterized by td + k where td is the treedepth of G (to be compared with the hardness for pathwidth 2 where k = 3). (We note that when k and r are unrestricted, the problem is trivially FPT parameterized by td.) Further, we derive as a corollary that strip packing is FPT with respect to the height of the strip plus the maximum of the dimensions of the packed rectangles, which was previously only known to be in XP. Second, we present a new parameterization, denoted aG, relating graph distance to geometric distance, which may be of independent interest. We show that the problem is para-NP-hard parameterized by aG, but FPT parameterized by aG on trees, as well as FPT parameterized by k + aG. Third, we show that the recognition of k × r grid graphs is NP-hard on graphs of pathwidth 2 where k = 3. Moreover, when k and r are unrestricted, we show that the problem is NP-hard on trees of pathwidth 2, but trivially solvable in polynomial time on graphs of pathwidth 1.

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“…Recently, the relationship between NP exposure and the risk of colorectal cancer progression has been a concern. The risk of colorectal cancer has significantly increased in populations living near the industries that release NP in Spain . Our previous study found a higher concentration of serum NP in patients with CRC than in healthy individuals in both men and women, and NP induced CRC cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

Nonylphenol Promoted Epithelial–Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle

Zhang

Yin

et al. 2022

Chem. Res. Toxicol.

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Nonylphenol (NP) is a widely used chemical, which has been considered a kind of endocrine-disrupting chemical and is involved in the occurrence and development of many types of cancers. Our recent studies demonstrated that NP exposure is related to colorectal cancer (CRC) progression. In this study, we also found epithelial–mesenchymal transition (EMT) promoted by NP treatment in CRC cells. However, the mechanism of NP on tumor metastasis is still unclear. In this study, we focused on the effect of the regulator of cell cycle (RGCC) induced by NP treatment. The cancer genome atlas (TCGA) analysis suggested that the expression of RGCC increased in CRC tissues, and our clinical samples showed that the expression of RGCC in tumor tissues is positively correlated with the serum level of NP in CRC patients. Further studies revealed that overexpression of RGCC could enhance the NP-induced EMT process in CRC cells and activate ERK signaling pathways. Inhibiting ERK signaling by ERK inhibitors or the knockdown of RGCC could attenuate the NP-induced EMT process. In addition, both RGCC overexpression and NP treatment could activate ERK pathways and attenuate the effect of ERK inhibitors on the EMT process in CRC cells. Altogether, this study demonstrated that NP could induce cell invasion and migration by increasing the expression of RGCC to enhance the EMT process, which might be through the activation of ERK signaling pathways. This finding supported a potential target for studying NP exposure-related colorectal cancers.

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Residential proximity to industrial pollution sources and colorectal cancer risk: A multicase-control study (MCC-Spain)

Cited by 35 publications

References 45 publications

Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2

Coiled-Coil Domain Containing 80 Suppresses Nonylphenol-Induced Colorectal Cancer Cell Proliferation by Inhibiting the Activation of ERK1/2

Grid Recognition: Classical and Parameterized Computational Perspectives

Nonylphenol Promoted Epithelial–Mesenchymal Transition in Colorectal Cancer Cells by Upregulating the Expression of Regulator of Cell Cycle

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