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Hyperglycemia, a neglected factor during cancer progression.

Duan W, Shen X, Lei J, Xu Q, Yu Y, Li R, Wu E, Ma Q - Biomed Res Int (2014)

Bottom Line: However, to date, the potential reasons for this association remain unclear.Considering associations between diabetes and malignancies, the effect of hyperglycemia on cancer progression in cancer patients with abnormal blood glucose should not be neglected.In this paper, we describe the role that hyperglycemia plays in cancer progression and treatment and illustrate that hyperglycemia may contribute to a more malignant phenotype of cancer cells and lead to drug resistance.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi 710061, China.

ABSTRACT
Recent evidence from large cohort studies suggests that there exists a higher cancer incidence in people with type 2 diabetes (DM2). However, to date, the potential reasons for this association remain unclear. Hyperglycemia, the most important feature of diabetes, may be responsible for the excess glucose supply for these glucose-hungry cells, and it contributes to apoptosis resistance, oncogenesis, and tumor cell resistance to chemotherapy. Considering associations between diabetes and malignancies, the effect of hyperglycemia on cancer progression in cancer patients with abnormal blood glucose should not be neglected. In this paper, we describe the role that hyperglycemia plays in cancer progression and treatment and illustrate that hyperglycemia may contribute to a more malignant phenotype of cancer cells and lead to drug resistance. Therefore, controlling hyperglycemia may have important therapeutic implications in cancer patients.

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Mechanism of high glucose-induced cellular events in cancer cells. High glucose (hyperglycemia) generates cellular ROS mainly through mitochondrial metabolism; elevated ROS activate MAPK cascade, which cause cellular events by inducing related genes transcription. In addition, high glucose can induce activation of protein kinase C (PKC) through direct and indirect pathways. It is also speculated that high glucose may induce EGF transcription and EGFR transactivation, contributing to various biological behavior of cancer cells. High glucose-mediated GDNF upregulation may also involve in different cellular events through GDNF/RET cascade.
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fig2: Mechanism of high glucose-induced cellular events in cancer cells. High glucose (hyperglycemia) generates cellular ROS mainly through mitochondrial metabolism; elevated ROS activate MAPK cascade, which cause cellular events by inducing related genes transcription. In addition, high glucose can induce activation of protein kinase C (PKC) through direct and indirect pathways. It is also speculated that high glucose may induce EGF transcription and EGFR transactivation, contributing to various biological behavior of cancer cells. High glucose-mediated GDNF upregulation may also involve in different cellular events through GDNF/RET cascade.

Mentions: Increased production of reactive oxygen species (ROS) from mitochondria is the main cause of hyperglycemic complications (Figure 2). In diabetic individuals, hyperglycemia in susceptible cells results in the overproduction of superoxide by the mitochondrial electron transport chain [36]. Elevated levels of ROS can lead to cellular DNA mutations and may, therefore, play an important role in the initiation and progression of multistage carcinogenesis. More importantly, the generation of ROS was required for K-Ras-induced anchorage-independent growth through regulation of the ERK MAPK signaling pathway [37].


Hyperglycemia, a neglected factor during cancer progression.

Duan W, Shen X, Lei J, Xu Q, Yu Y, Li R, Wu E, Ma Q - Biomed Res Int (2014)

Mechanism of high glucose-induced cellular events in cancer cells. High glucose (hyperglycemia) generates cellular ROS mainly through mitochondrial metabolism; elevated ROS activate MAPK cascade, which cause cellular events by inducing related genes transcription. In addition, high glucose can induce activation of protein kinase C (PKC) through direct and indirect pathways. It is also speculated that high glucose may induce EGF transcription and EGFR transactivation, contributing to various biological behavior of cancer cells. High glucose-mediated GDNF upregulation may also involve in different cellular events through GDNF/RET cascade.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4016871&req=5

fig2: Mechanism of high glucose-induced cellular events in cancer cells. High glucose (hyperglycemia) generates cellular ROS mainly through mitochondrial metabolism; elevated ROS activate MAPK cascade, which cause cellular events by inducing related genes transcription. In addition, high glucose can induce activation of protein kinase C (PKC) through direct and indirect pathways. It is also speculated that high glucose may induce EGF transcription and EGFR transactivation, contributing to various biological behavior of cancer cells. High glucose-mediated GDNF upregulation may also involve in different cellular events through GDNF/RET cascade.
Mentions: Increased production of reactive oxygen species (ROS) from mitochondria is the main cause of hyperglycemic complications (Figure 2). In diabetic individuals, hyperglycemia in susceptible cells results in the overproduction of superoxide by the mitochondrial electron transport chain [36]. Elevated levels of ROS can lead to cellular DNA mutations and may, therefore, play an important role in the initiation and progression of multistage carcinogenesis. More importantly, the generation of ROS was required for K-Ras-induced anchorage-independent growth through regulation of the ERK MAPK signaling pathway [37].

Bottom Line: However, to date, the potential reasons for this association remain unclear.Considering associations between diabetes and malignancies, the effect of hyperglycemia on cancer progression in cancer patients with abnormal blood glucose should not be neglected.In this paper, we describe the role that hyperglycemia plays in cancer progression and treatment and illustrate that hyperglycemia may contribute to a more malignant phenotype of cancer cells and lead to drug resistance.

View Article: PubMed Central - PubMed

Affiliation: Department of Hepatobiliary Surgery, First Affiliated Hospital, Medical College, Xi'an Jiaotong University, 277 West Yanta Road, Xi'an, Shaanxi 710061, China.

ABSTRACT
Recent evidence from large cohort studies suggests that there exists a higher cancer incidence in people with type 2 diabetes (DM2). However, to date, the potential reasons for this association remain unclear. Hyperglycemia, the most important feature of diabetes, may be responsible for the excess glucose supply for these glucose-hungry cells, and it contributes to apoptosis resistance, oncogenesis, and tumor cell resistance to chemotherapy. Considering associations between diabetes and malignancies, the effect of hyperglycemia on cancer progression in cancer patients with abnormal blood glucose should not be neglected. In this paper, we describe the role that hyperglycemia plays in cancer progression and treatment and illustrate that hyperglycemia may contribute to a more malignant phenotype of cancer cells and lead to drug resistance. Therefore, controlling hyperglycemia may have important therapeutic implications in cancer patients.

Show MeSH
Related in: MedlinePlus