Imbalance in leptin-adiponectin levels and leptin receptor expression as chief contributors to triple negative breast cancer progression in Northeast India

Sultana, Rizwana; Kataki, Amal Ch; Borthakur, Bibhuti Bhusan; Basumatary, Tarun Kumar; Bose, Sujoy

doi:10.1016/j.gene.2017.04.021

Cited by 41 publications

(25 citation statements)

References 51 publications

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“…Both are secreted primarily by adipose tissue, increase with higher degrees of adiposity, and has been implicated for their role in obesity, inflammation, and breast tumorigenesis (51)(52)(53). Breast cancer patients are characterized by high serum leptin concentrations as well as increased leptin receptor expression especially in higher pathological grade tumor tissues and patients who develop resistance to anti-cancer treatments (54,55). Both leptin and resistin exacerbates an inflammatory microenvironment by favoring the secretion of other pro-inflammatory adipokines.…”

Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 99%

“…Additionally, leptin favors breast cancer progression by inducing cellular proliferation by binding to its receptor followed by downstream signaling through NFκB, STAT3, ERK1/ERK2, and phosphoinositide-3-kinase (PI3K) pathways (56,57). Both elevated leptin and resistin concentrations was associated with the promotion of cancer stem cell survival and the promotion of invasion and migration via epithelial to mesenchymal transition in breast cancer cells (55,56,58), which contributes to the development of treatment resistance.…”

Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 99%

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Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

et al. 2020

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Breast cancer cells modulate lipid and fatty acid metabolism to sustain proliferation. The role of adipocytes in cancer treatment efficacy remains, however, to be fully elucidated. We investigated whether diet-induced obesity (DIO) affects the efficacy of doxorubicin treatment in a breast tumor-bearing mouse model. Female C57BL6 mice were fed a high fat or low fat diet for the full duration of the study (12 weeks). After 8 weeks, mice were inoculated with E0771 triple-negative breast cancer cells in the fourth mammary gland to develop breast tumor allographs. Tumor-bearing mice received either vehicle (Hank's balanced salt solution) or doxorubicin (chemotherapy). Plasma inflammatory markers, tumor, and mammary adipose tissue fatty acid composition, as well as protein expression of lipid metabolism markers were determined. The high fat diet (HFD) attenuated the treatment efficacy of doxorubicin. Both leptin and resistin concentrations were significantly increased in the HFD group treated with doxorubicin. Suppressed lipogenesis (decreased stearoyl CoA-desaturase-1) and lipolysis (decreased hormone-sensitive lipase) were observed in mammary adipose tissue of the DIO animals, whereas increased expression was observed in the tumor tissue of doxorubicin treated HFD mice. Obesogenic conditions induced altered tissue fatty acid (FA) compositions, which reduced doxorubicin's treatment efficacy. In mammary adipose tissue breast cancer cells suppressed the storage of FAs, thereby increasing the availability of free FAs and favored inflammation under obesogenic conditions.

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Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 99%

Section: Inflammatory Markers: Diet-induced Obesity Induces Systemic mentioning

confidence: 99%

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

et al. 2020

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“…16 Emerging evidence has proposed that human homeobox protein (Nanog) is a excellent target in cancer therapy owing to its regulation of cancer cell proliferation, metastasis and apoptosis. 17 In addition, Nanog plays a crucial role in maintaining the stemness of cancer cells, such as self-renewal, recurrence and high tumorigenicity in various cancers. 18 Previous researches have reported that inhibition of Nanog functions was capable of suppressing cancer cell growth and inducing cancer cell apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Novel functionalized nanoparticles for tumor-targeting co-delivery of doxorubicin and siRNA to enhance cancer therapy

Xia

Wang

et al. 2017

IJN

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Human homeobox protein (Nanog) is highly expressed in most cancer cells and has gradually emerged as an excellent target in cancer therapy, owing to its regulation of cancer cell proliferation, metastasis and apoptosis. In this study, we prepared tumor-targeting functionalized selenium nanoparticles (RGDfC-SeNPs) to load chemotherapeutic doxorubicin (DOX) and Nanog siRNA. Herein, RGDfC peptide was used as a tumor-targeting moiety which could specifically bind to α v β 3 integrins overexpressed on various cancer cells. The sizes of RGDfC-SeNPs@DOX nanoparticles (~12 nm) were confirmed by both dynamic light scattering and transmission electron microscopy. The chemical structure of RGDfC-SeNPs@DOX was characterized via Fourier-transform infrared spectroscopy. The RGDfC-SeNPs@DOX was compacted with siRNA (anti-Nanog) by electrostatic interaction to fabricate the RGDfC-SeNPs@DOX/siRNA complex. The RGDfC-SeNPs@DOX/siRNA complex nanoparticles could efficiently enter into HepG2 cells via clathrin-associated endocytosis, and showed high gene transfection efficiency that resulted in enhanced gene silencing. The in vivo biodistribution experiment indicated that RGDfC-SeNPs@DOX/siRNA nanoparticles were capable of specifically accumulating in the tumor site. Furthermore, treatment with RGDfC-SeNPs@DOX/siRNA resulted in a more significant anticancer activity than the free DOX, RGDfC-SeNPs@DOX or RGDfC-SeNPs/siRNA in vitro and in vivo. In summary, this study shows a novel type of DOX and siRNA co-delivery system, thereby providing an alternative route for cancer treatment.

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“…Another study has demonstrated that free fatty acids added to co-cultures of breast cancer cells and adipocytes were transferred to cancer cells, driving fatty acid metabolism, resulting in increased proliferation and cell migration [138]. The upgraded serum levels of leptin have also been associated with higher pathological grade and aggressive phenotypes in breast cancer patients [139]. Produced by adipose tissues, IL-6 is more secreted in CAAs compared with other adipocytes [131], and it has also been shown to promote cancer progression when adipocytes are co-cultured with breast cancer cells [140].…”

Section: Cancer-associated Adipocytesmentioning

confidence: 99%

“…Pathobiology 2020;87:[125][126][127][128][129][130][131][132][133][134][135][136][137][138][139][140][141][142] …”

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The Multifaceted Nature of Tumor Microenvironment in Breast Carcinomas

et al. 2020

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Heterogeneity in breast carcinomas can be appreciated at various levels, from morphology to molecular alterations, and there are well-known genotypic-phenotypic correlations. Clinical decision-making is strictly focused on the evaluation of tumor cells and is based on the assessment of hormone receptors and of the HER2 status, by means of a combination of immunohistochemical and in situ hybridization techniques. The tumor microenvironment (TME) also shows a multifaceted nature stemming from the different actors populating the intratumoral and the peritumoral stroma of breast carcinomas. Of note, we have now evidence that tumor-infiltrating lymphocytes (TILs) are clinically meaningful as their quantification in the intratumoral stroma strongly correlates with good prognosis, in particular in triple-negative and HER2-positive breast cancer patients. Nevertheless, TILs are just one of the many actors orchestrating the com-plexity of the TME, which is populated by immune and nonimmune cells (cancer-associated fibroblasts, cancer-associated adipocytes), as well as non-cellular components such as chemical inflammation mediators. In this review article we will overview the main features of the distinct cell compartments by discussing (i) the potential impact the TME may have on the prognostic stratification of breast cancers and (ii) the possible predictive value of some markers in the context of immunotherapy in light of the recent results of phase III studies in advanced and early triple-negative breast cancer patients.

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Imbalance in leptin-adiponectin levels and leptin receptor expression as chief contributors to triple negative breast cancer progression in Northeast India

Cited by 41 publications

References 51 publications

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

Decreased Efficacy of Doxorubicin Corresponds With Modifications in Lipid Metabolism Markers and Fatty Acid Profiles in Breast Tumors From Obese vs. Lean Mice

Novel functionalized nanoparticles for tumor-targeting co-delivery of doxorubicin and siRNA to enhance cancer therapy

The Multifaceted Nature of Tumor Microenvironment in Breast Carcinomas

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