Hyperglycemia and Chemoresistance in Breast Cancer: From Cellular Mechanisms to Treatment Response

Qiu, Jie; Zheng, Qinghui; Meng, Xuli

doi:10.3389/fonc.2021.628359

Cited by 36 publications

(38 citation statements)

References 103 publications

(100 reference statements)

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“…INS is one of the key growth factors for many types of neoplastic cells [32][33][34][35][36][37][38][39][40], and it is a potent growth factor for myeloma cells [20]. Our data fully confirm these dates and show that INS enhances serum-induced proliferation of RPMI8226 and IM9 cells (Figure 2A and Figure 2B).…”

Section: Effects Of Ins On the Cas-3 And Bcl-2 Mrna Expression Levelssupporting

confidence: 82%

Untitled

2021

Biointerface Res Appl Chem

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Many reports have documented the role of INS (insulin) as growth factors in a variety of cancers. Epidemiological studies revealed that INS therapy causes increased mortality in multiple myeloma (MM) patients with pre-existing or steroid-induced type 2 diabetes. However, there is limited experimental evidence of this association. In the present study, the dual effect of INS on the viability of myeloma RPMI8226 and lymphoblastoid IM9 cells was revealed. In serum-containing medium exogenous INS serves as a growth factor, whereas INS decreases the number of cells under serum-free medium. In the last case, the main mechanism of decreasing the cell population is apoptosis through up-regulation of Cas-3 and downregulation of Bcl-2 expression. INS has also been shown to be involved in the regulation of necrotic cell death.

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Section: Effects Of Ins On the Cas-3 And Bcl-2 Mrna Expression Levelssupporting

confidence: 82%

Untitled

2021

Biointerface Res Appl Chem

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“…In liver cancer, elevated level of nitric oxide is linked with growth arrest and apoptosis along with chemosensitization through modulated levels of p53 and HIF-1a (42). Curcuminmediated increased extracellular pH and decreased lactate can also be correlated with augmented sensitivity towards anticancer drugs (5,6). Previously, lactate was reported to enhance the chemoresistance in cancer cells (14,43).…”

Section: Discussionmentioning

confidence: 99%

“…High level of glucose favored the proliferation along with a significant decline in the number of dead cells; and triggered the resistance and druginduced cell death in hepatic carcinoma cells. Hyperglycemic conditions incept the chemoresistant phenotype in a variety of malignant cells (4,6,8,9,37). Modulation of various molecular regulators of cell survival was reported to play a critical role in high glucose-triggered chemoresistance (6,24,37).…”

Section: Discussionmentioning

confidence: 99%

“…Hyperglycemic conditions incept the chemoresistant phenotype in a variety of malignant cells (4,6,8,9,37). Modulation of various molecular regulators of cell survival was reported to play a critical role in high glucose-triggered chemoresistance (6,24,37). A significant decline in the expression of p53 was observed in HepG2 cells treated with high glucose level.…”

Section: Discussionmentioning

confidence: 99%

“…The "aerobic glycolysis" (Warburg effect) also serves as a landscape for the selection of aggressive cancer cells (5). Moreover, a hyperglycemic condition in the extracellular milieu has been shown to confer advantages to cancer cells including the onset of chemoresistance (4,(6)(7)(8)(9). In a comparison of meta-analyses, Li et al (9) reported highest relative risk for liver cancer in diabetic patients (9).…”

Section: Introductionmentioning

confidence: 99%

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Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells

et al. 2021

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Along with direct anticancer activity, curcumin hinders the onset of chemoresistance. Among many, high glucose condition is a key driving factor for chemoresistance. However, the ability of curcumin remains unexplored against high glucose-induced chemoresistance. Moreover, chemoresistance is major hindrance in effective clinical management of liver cancer. Using hepatic carcinoma HepG2 cells, the present investigation demonstrates that high glucose induces chemoresistance, which is averted by the simultaneous presence of curcumin. Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production. Modulated molecular regulators are suggested to play a crucial role as curcumin pretreatment also prevented the onset of chemoresistance by high glucose. High glucose instigated suppression in the intracellular accumulation of anticancer drug doxorubicin and drug-induced chromatin compactness along with declined expression of drug efflux pump MDR-1 and transcription factors and signal transducers governing the survival, aggressiveness, and apoptotic cell death (p53, HIF-1α, mTOR, MYC, STAT3). Curcumin alleviated the suppression of drug retention and nuclear condensation along with hindering the high glucose-induced alterations in transcription factors and signal transducers. High glucose-driven resistance in cancer cells was associated with elevated expression of metabolic enzymes HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, transporters, and receptors in cancer cells. Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition. Taken together, the findings of the present investigation first time demonstrate the ability of curcumin against high glucose-induced chemoresistance, along with its molecular mechanism. This will have implication in therapeutic management of malignancies in diabetic conditions.

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Global burden of female breast cancer and its association with socioeconomic development status, 1990–2044

Zhang

et al. 2023

Cancer Reports

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BackgroundBreast cancer is a widespread disease in women worldwide.AimWe aimed to explore the global epidemiological trends of female breast cancer (FBC) between 1990 and 2044.Methods and ResultsDisease burden, population, and socio‐demographic index (SDI) data were obtained from the Global Health Data Exchange (GHDx) database. We analyzed temporal trends, age differences, risk factors, and geographic patterns of FBC disease burden globally and explored the association between age‐standardized incidence rate (ASIR) of FBC and SDI. Bayesian age‐period‐cohort model was also performed to predict the changes in FBC incidence worldwide from 2020 to 2044. First, the global ASIR of FBC increased by 14.31% from 1990 to 2019 (95% Uncertainty Interval 4.75% to 23.98%). The death rate presented a falling trend. Second, alcohol use is the most‐highlighted risk factor for FBC in some high‐income regions such as Europe. A high fasting plasma glucose levels is the most prominent risk factor for FBC in Latin America and Africa. Third, the ASIR of the FBC increases with the SDI. Fourth, the incidence is expected to increase faster among women aged 35–60 years and fastest for those aged 50–54 years from 2020 to 2044. Countries with a high incidence of FBC that is expected to increase significantly include Barbados, Burkina Faso, Senegal, Monaco, Lebanon, Togo, and Uganda.ConclusionThe disease burden of FBC varies worldwide; the findings suggest attaching importance to the control of middle and low‐middle SDI regions. Public health as well as cancer prevention experts should pay more attention to regions and populations at an increased risk of developing FBC, focusing on their prevention and rehabilitation while conducting further epidemiological studies to investigate the risk factors of their increase.

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Hyperglycemia and Chemoresistance in Breast Cancer: From Cellular Mechanisms to Treatment Response

Cited by 36 publications

References 103 publications

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Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells

Global burden of female breast cancer and its association with socioeconomic development status, 1990–2044

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