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Article ; Online: Roles of citrus fruits on energy expenditure, body weight management, and metabolic biomarkers: a comprehensive review.

Aslan, Merve Nur / Sukan-Karaçağıl, Betül / Acar-Tek, Nilüfer

2023

Abstract: Citrus fruits are widely consumed for their nutritional and health benefits. They belong to the Rutaceae and have many varieties, such as sweet orange (Citrus sinensis), which is the most popular. Citrus fruits are rich in water (>80%), dietary fiber, ... ...

Abstract	Citrus fruits are widely consumed for their nutritional and health benefits. They belong to the Rutaceae and have many varieties, such as sweet orange (Citrus sinensis), which is the most popular. Citrus fruits are rich in water (>80%), dietary fiber, and vitamins. They also contain bioactive components, which may modulate energy metabolism and lipid oxidation through various mechanisms. These mechanisms include stimulating β3-adrenergic receptors, increasing mitochondrial biogenesis and thermogenesis, activating AMP kinase and peroxisome proliferator-activated receptor-gamma coactivator-1α pathways, inhibiting lipogenesis and lipid accumulation, and inducing browning of white adipose tissue. This review summarizes the mechanisms and outcomes of citrus fruits and their metabolites on energy metabolism and body weight in different experimental models. The literature was searched for in vitro and in vivo animal and human studies that investigated the effects of citrus consumption on energy expenditure, thermogenesis, adipogenesis, and lipid accumulation. Citrus fruits and their metabolites have shown promising effects on energy metabolism and lipid oxidation in in vitro and in vivo animal studies. However, the evidence from human studies is limited and inconsistent. Possible reasons for the discrepancy are briefly discussed, and knowledge gaps and research needs are identified for future studies. Citrus fruits may have beneficial effects on energy metabolism and body weight, but more rigorous and well-designed human trials are needed to confirm their efficacy and safety.
Language	English
Publishing date	2023-09-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	82067-2
ISSN	1753-4887 ; 0029-6643
ISSN (online)	1753-4887
ISSN	0029-6643
DOI	10.1093/nutrit/nuad116
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Article ; Online: TRAK adaptors regulate the recruitment and activation of dynein and kinesin in mitochondrial transport.

Canty, John T / Hensley, Andrew / Aslan, Merve / Jack, Amanda / Yildiz, Ahmet

Nature communications

2023 Volume 14, Issue 1, Page(s) 1376

Abstract: Mitochondrial transport along microtubules is mediated by Miro1 and TRAK adaptors that recruit kinesin-1 and dynein-dynactin. To understand how these opposing motors are regulated during mitochondrial transport, we reconstitute the bidirectional ... ...

Abstract	Mitochondrial transport along microtubules is mediated by Miro1 and TRAK adaptors that recruit kinesin-1 and dynein-dynactin. To understand how these opposing motors are regulated during mitochondrial transport, we reconstitute the bidirectional transport of Miro1/TRAK along microtubules in vitro. We show that the coiled-coil domain of TRAK activates dynein-dynactin and enhances the motility of kinesin-1 activated by its cofactor MAP7. We find that TRAK adaptors that recruit both motors move towards kinesin-1's direction, whereas kinesin-1 is excluded from binding TRAK transported by dynein-dynactin, avoiding motor tug-of-war. We also test the predictions of the models that explain how mitochondrial transport stalls in regions with elevated Ca
MeSH term(s)	Dyneins/metabolism ; Kinesins/metabolism ; Dynactin Complex/metabolism ; Microtubules/metabolism ; Biological Transport ; Microtubule-Associated Proteins/metabolism
Chemical Substances	Dyneins (EC 3.6.4.2) ; Kinesins (EC 3.6.4.4) ; Dynactin Complex ; Microtubule-Associated Proteins
Language	English
Publishing date	2023-03-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-36945-8
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Article ; Online: Quantifying the invasion and migration ability of cancer cells with a 3D Matrigel drop invasion assay.

Aslan, Merve / Hsu, En-Chi / Liu, Shiqin / Stoyanova, Tanya

Biology methods & protocols

2021 Volume 6, Issue 1, Page(s) bpab014

Abstract: Metastasis is the main cause of cancer-associated morbidity which will account for ∼ 600,000 deaths in the USA in 2021. Defining new mechanisms that drive cancer metastasis is vital for developing new therapeutic strategies and improving clinical ... ...

Abstract	Metastasis is the main cause of cancer-associated morbidity which will account for ∼ 600,000 deaths in the USA in 2021. Defining new mechanisms that drive cancer metastasis is vital for developing new therapeutic strategies and improving clinical outcomes for cancer patients. Herein, we describe a recently established 3D Matrigel drop invasion assay to measure cancer cell invasion and migration capability
Language	English
Publishing date	2021-07-21
Publishing country	England
Document type	Journal Article
ISSN	2396-8923
ISSN (online)	2396-8923
DOI	10.1093/biomethods/bpab014
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Article ; Online: Metastasis Model to Test the Role of Notch Signaling in Prostate Cancer.

Liu, Shiqin / Hsu, En-Chi / Shen, Michelle / Aslan, Merve / Stoyanova, Tanya

Methods in molecular biology (Clifton, N.J.)

2022 Volume 2472, Page(s) 221–233

Abstract: Distant metastasis is the main cause of death in prostate cancer patients. Notch signaling plays an important role in driving prostate cancer aggressiveness and metastasis. In this chapter, we describe a protocol to measure prostate cancer metastatic ... ...

Abstract	Distant metastasis is the main cause of death in prostate cancer patients. Notch signaling plays an important role in driving prostate cancer aggressiveness and metastasis. In this chapter, we describe a protocol to measure prostate cancer metastatic colonization, incidences of metastasis, accurately quantify the burden of metastasis, and test the role of NOTCH1 receptor on prostate cancer metastatic colonization and homing to distant sites. The metastasis model presented here is established by intracardiac injection of control human prostate cancer cells and NOTCH1 downregulated cells. The cells are engineered to express both red fluorescent protein (RFP) and luciferase. In this model, whole body bioluminescence imaging, high-resolution, and quantitative fluorescence imaging are utilized for quantitative assessment of metastatic colonization and metastasis burden. Further, histopathology analyses of diverse metastatic organs are performed. This model is a powerful and versatile tool to investigate the mechanisms underlying the function of NOTCH receptors in metastatic colonization in prostate cancer.
MeSH term(s)	Cell Line, Tumor ; Humans ; Male ; Neoplasm Metastasis ; Prostatic Neoplasms/pathology ; Receptor, Notch1/genetics ; Receptor, Notch1/metabolism ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction
Chemical Substances	Receptor, Notch1 ; Receptors, Notch
Language	English
Publishing date	2022-06-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-0716-2201-8_18
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Article ; Online: Co-axial hydrogel spinning for facile biofabrication of prostate cancer-like 3D models.

Guimarães, Carlos F / Liu, Shiqin / Wang, Jie / Purcell, Emma / Ozedirne, Tugba / Ren, Tanchen / Aslan, Merve / Yin, Qingqing / Reis, Rui L / Stoyanova, Tanya / Demirci, Utkan

Biofabrication

2024 Volume 16, Issue 2

Abstract: Glandular cancers are amongst the most prevalent types of cancer, which can develop in many different organs, presenting challenges in their detection as well as high treatment variability and failure rates. For that purpose, anticancer drugs are ... ...

Abstract	Glandular cancers are amongst the most prevalent types of cancer, which can develop in many different organs, presenting challenges in their detection as well as high treatment variability and failure rates. For that purpose, anticancer drugs are commonly tested in cancer cell lines grown in 2D tissue culture on plastic dishes
MeSH term(s)	Humans ; Animals ; Male ; Hydrogels/chemistry ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Cell Line
Chemical Substances	Hydrogels ; Antineoplastic Agents
Language	English
Publishing date	2024-02-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2500944-8
ISSN	1758-5090 ; 1758-5082
ISSN (online)	1758-5090
ISSN	1758-5082
DOI	10.1088/1758-5090/ad2535
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Article ; Online: Ferroptosis Inducers Are a Novel Therapeutic Approach for Advanced Prostate Cancer.

Ghoochani, Ali / Hsu, En-Chi / Aslan, Merve / Rice, Meghan A / Nguyen, Holly M / Brooks, James D / Corey, Eva / Paulmurugan, Ramasamy / Stoyanova, Tanya

Cancer research

2021 Volume 81, Issue 6, Page(s) 1583–1594

Abstract: Ferroptosis is a type of programmed cell death induced by the accumulation of lipid peroxidation and lipid reactive oxygen species in cells. It has been recently demonstrated that cancer cells are vulnerable to ferroptosis inducers (FIN). However, the ... ...

Abstract	Ferroptosis is a type of programmed cell death induced by the accumulation of lipid peroxidation and lipid reactive oxygen species in cells. It has been recently demonstrated that cancer cells are vulnerable to ferroptosis inducers (FIN). However, the therapeutic potential of FINs in prostate cancer in preclinical settings has not been explored. In this study, we demonstrate that mediators of ferroptosis, solute carrier family 7 member 11, SLC3A2, and glutathione peroxidase, are expressed in treatment-resistant prostate cancer. We further demonstrate that treatment-resistant prostate cancer cells are sensitive to two FINs, erastin and RSL3. Treatment with erastin and RSL3 led to a significant decrease in prostate cancer cell growth and migration
MeSH term(s)	Amino Acid Transport System y+/metabolism ; Androgen Antagonists/pharmacology ; Androgen Antagonists/therapeutic use ; Androstenes/pharmacology ; Androstenes/therapeutic use ; Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Benzamides/pharmacology ; Benzamides/therapeutic use ; Carbolines/pharmacology ; Carbolines/therapeutic use ; Cell Line, Tumor ; Drug Resistance, Neoplasm/drug effects ; Ferroptosis/drug effects ; Fusion Regulatory Protein 1, Heavy Chain/metabolism ; Humans ; Male ; Mice ; Neoplasm Staging ; Nitriles/pharmacology ; Nitriles/therapeutic use ; Phenylthiohydantoin/pharmacology ; Phenylthiohydantoin/therapeutic use ; Phospholipid Hydroperoxide Glutathione Peroxidase/metabolism ; Piperazines/pharmacology ; Piperazines/therapeutic use ; Prostate/pathology ; Prostatic Neoplasms, Castration-Resistant/diagnosis ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/pathology ; Xenograft Model Antitumor Assays
Chemical Substances	Amino Acid Transport System y+ ; Androgen Antagonists ; Androstenes ; Benzamides ; Carbolines ; Fusion Regulatory Protein 1, Heavy Chain ; Nitriles ; Piperazines ; RSL3 compound ; SLC3A2 protein, human ; SLC7A11 protein, human ; erastin ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU) ; Phospholipid Hydroperoxide Glutathione Peroxidase (EC 1.11.1.12) ; abiraterone (G819A456D0)
Language	English
Publishing date	2021-01-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-20-3477
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Article ; Online: Loss of Notch1 Activity Inhibits Prostate Cancer Growth and Metastasis and Sensitizes Prostate Cancer Cells to Antiandrogen Therapies.

Rice, Meghan A / Hsu, En-Chi / Aslan, Merve / Ghoochani, Ali / Su, Austin / Stoyanova, Tanya

Molecular cancer therapeutics

2019 Volume 18, Issue 7, Page(s) 1230–1242

Abstract: Prostate cancer remains among the leading causes of cancer-related deaths in men. Patients with aggressive disease typically undergo hormone deprivation therapy. Although treatment is initially very successful, these men commonly progress to lethal, ... ...

Abstract	Prostate cancer remains among the leading causes of cancer-related deaths in men. Patients with aggressive disease typically undergo hormone deprivation therapy. Although treatment is initially very successful, these men commonly progress to lethal, castration-resistant prostate cancer (CRPC) in 2 to 3 years. Standard therapies for CRPC include second-generation antiandrogens, which prolong patient lifespan by only several months. It is imperative to advance our understanding of the mechanisms leading to resistance to identify new therapies for aggressive prostate cancer. This study identifies Notch1 as a therapeutic target in prostate cancer. Loss of
MeSH term(s)	Androgen Antagonists/pharmacology ; Androgen Antagonists/therapeutic use ; Animals ; Cell Line, Tumor ; Humans ; Male ; Mice ; Neoplasm Metastasis ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/pathology ; Receptor, Notch1/genetics
Chemical Substances	Androgen Antagonists ; NOTCH1 protein, human ; Receptor, Notch1
Language	English
Publishing date	2019-04-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2063563-1
ISSN	1538-8514 ; 1535-7163
ISSN (online)	1538-8514
ISSN	1535-7163
DOI	10.1158/1535-7163.MCT-18-0804
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Zs.A 5750: Show issues

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Article ; Online: ACAA2 is a novel molecular indicator for cancers with neuroendocrine phenotype.

Shen, Michelle / Liu, Shiqin / Toland, Angus / Hsu, En-Chi / Hartono, Alifiani B / Alabi, Busola R / Aslan, Merve / Nguyen, Holly M / Sessions, Conner J / Nolley, Rosalie / Shi, Chanjuan / Huang, Jiaoti / Brooks, James D / Corey, Eva / Stoyanova, Tanya

British journal of cancer

2023 Volume 129, Issue 11, Page(s) 1818–1828

Abstract: Background: Neuroendocrine phenotype is commonly associated with therapy resistance and poor prognoses in small-cell neuroendocrine cancers (SCNCs), such as neuroendocrine prostate cancer (NEPC) and small-cell lung cancer (SCLC). Expression levels of ... ...

Abstract	Background: Neuroendocrine phenotype is commonly associated with therapy resistance and poor prognoses in small-cell neuroendocrine cancers (SCNCs), such as neuroendocrine prostate cancer (NEPC) and small-cell lung cancer (SCLC). Expression levels of current neuroendocrine markers exhibit high case-by-case variability, so multiple markers are used in combination to identify SCNCs. Here, we report that ACAA2 is elevated in SCNCs and is a potential molecular indicator for SCNCs. Methods: ACAA2 expressions in tumour xenografts, tissue microarrays (TMAs), and patient tissues from prostate and lung cancers were analysed via immunohistochemistry. ACAA2 mRNA levels in lung and prostate cancer (PC) patients were assessed in published datasets. Results: ACAA2 protein and mRNA levels were elevated in SCNCs relative to non-SCNCs. Medium/high ACAA2 intensity was observed in 78% of NEPC PDXs samples (N = 27) relative to 33% of adeno-CRPC (N = 86), 2% of localised PC (N = 50), and 0% of benign prostate specimens (N = 101). ACAA2 was also elevated in lung cancer patient tissues with neuroendocrine phenotype. 83% of lung carcinoid tissues (N = 12) and 90% of SCLC tissues (N = 10) exhibited medium/high intensity relative to 40% of lung adenocarcinoma (N = 15). Conclusion: ACAA2 expression is elevated in aggressive SCNCs such as NEPC and SCLC, suggesting it is a potential molecular indicator for SCNCs.
MeSH term(s)	Humans ; Male ; Carcinoma, Neuroendocrine/pathology ; Carcinoma, Small Cell/genetics ; Cell Line, Tumor ; Lung Neoplasms/genetics ; Phenotype ; Prostatic Neoplasms/pathology ; RNA, Messenger ; Small Cell Lung Carcinoma/genetics
Chemical Substances	RNA, Messenger ; ACAA2 protein, human (EC 2.3.1.16)
Language	English
Publishing date	2023-10-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-023-02448-y
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Article ; Online: UCHL1 is a potential molecular indicator and therapeutic target for neuroendocrine carcinomas.

Liu, Shiqin / Chai, Timothy / Garcia-Marques, Fernando / Yin, Qingqing / Hsu, En-Chi / Shen, Michelle / Shaw Toland, Angus Martin / Bermudez, Abel / Hartono, Alifiani B / Massey, Christopher F / Lee, Chung S / Zheng, Liwei / Baron, Maya / Denning, Caden J / Aslan, Merve / Nguyen, Holly M / Nolley, Rosalie / Zoubeidi, Amina / Das, Millie /

Kunder, Christian A / Howitt, Brooke E / Soh, H Tom / Weissman, Irving L / Liss, Michael A / Chin, Arnold I / Brooks, James D / Corey, Eva / Pitteri, Sharon J / Huang, Jiaoti / Stoyanova, Tanya

Cell reports. Medicine

2024 Volume 5, Issue 2, Page(s) 101381

Abstract: Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is ... ...

Abstract	Neuroendocrine carcinomas, such as neuroendocrine prostate cancer and small-cell lung cancer, commonly have a poor prognosis and limited therapeutic options. We report that ubiquitin carboxy-terminal hydrolase L1 (UCHL1), a deubiquitinating enzyme, is elevated in tissues and plasma from patients with neuroendocrine carcinomas. Loss of UCHL1 decreases tumor growth and inhibits metastasis of these malignancies. UCHL1 maintains neuroendocrine differentiation and promotes cancer progression by regulating nucleoporin, POM121, and p53. UCHL1 binds, deubiquitinates, and stabilizes POM121 to regulate POM121-associated nuclear transport of E2F1 and c-MYC. Treatment with the UCHL1 inhibitor LDN-57444 slows tumor growth and metastasis across neuroendocrine carcinomas. The combination of UCHL1 inhibitors with cisplatin, the standard of care used for neuroendocrine carcinomas, significantly delays tumor growth in pre-clinical settings. Our study reveals mechanisms of UCHL1 function in regulating the progression of neuroendocrine carcinomas and identifies UCHL1 as a therapeutic target and potential molecular indicator for diagnosing and monitoring treatment responses in these malignancies.
MeSH term(s)	Male ; Humans ; Ubiquitin Thiolesterase/genetics ; Ubiquitin Thiolesterase/metabolism ; Carcinoma, Neuroendocrine/drug therapy ; Carcinoma, Neuroendocrine/genetics ; Small Cell Lung Carcinoma ; Lung Neoplasms/diagnosis ; Lung Neoplasms/drug therapy ; Membrane Glycoproteins
Chemical Substances	Ubiquitin Thiolesterase (EC 3.4.19.12) ; POM121 protein, human ; Membrane Glycoproteins ; UCHL1 protein, human
Language	English
Publishing date	2024-01-19
Publishing country	United States
Document type	Journal Article
ISSN	2666-3791
ISSN (online)	2666-3791
DOI	10.1016/j.xcrm.2023.101381
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Article ; Online: Discovery of CASP8 as a potential biomarker for high-risk prostate cancer through a high-multiplex immunoassay.

Liu, Shiqin / Garcia-Marques, Fernando / Zhang, Chiyuan Amy / Lee, Jordan John / Nolley, Rosalie / Shen, Michelle / Hsu, En-Chi / Aslan, Merve / Koul, Kashyap / Pitteri, Sharon J / Brooks, James D / Stoyanova, Tanya

Scientific reports

2021 Volume 11, Issue 1, Page(s) 7612

Abstract: Prostate cancer remains the most common non-cutaneous malignancy among men in the United States. To discover potential serum-based biomarkers for high-risk prostate cancer, we performed a high-multiplex immunoassay utilizing patient-matched pre-operative ...

Abstract	Prostate cancer remains the most common non-cutaneous malignancy among men in the United States. To discover potential serum-based biomarkers for high-risk prostate cancer, we performed a high-multiplex immunoassay utilizing patient-matched pre-operative and post-operative serum samples from ten men with high-grade and high-volume prostate cancer. Our study identified six (CASP8, MSLN, FGFBP1, ICOSLG, TIE2 and S100A4) out of 174 proteins that were significantly decreased after radical prostatectomy. High levels of CASP8 were detected in pre-operative serum samples when compared to post-operative serum samples and serum samples from patients with benign prostate hyperplasia (BPH). By immunohistochemistry, CASP8 protein was expressed at higher levels in prostate cancer tissues compared to non-cancerous and BPH tissues. Likewise, CASP8 mRNA expression was significantly upregulated in prostate cancer when compared to benign prostate tissues in four independent clinical datasets. In addition, mRNA levels of CASP8 were higher in patients with recurrent prostate cancer when compared to patients with non-recurrent prostate cancer and high expression of CASP8 was associated with worse disease-free survival and overall survival in renal cancer. Together, our results suggest that CASP8 may potentially serve as a biomarker for high-risk prostate cancer and possibly renal cancer.
MeSH term(s)	Aged ; Biomarkers, Tumor/blood ; Caspase 8/genetics ; Caspase 8/metabolism ; Disease-Free Survival ; Humans ; Immunoassay/methods ; Immunohistochemistry/methods ; Immunologic Tests/methods ; Male ; Middle Aged ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/metabolism ; Prostate/pathology ; Prostate-Specific Antigen/blood ; Prostatectomy ; Prostatic Hyperplasia/metabolism ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/metabolism ; Risk Factors
Chemical Substances	Biomarkers, Tumor ; Prostate-Specific Antigen (EC 3.4.21.77) ; CASP8 protein, human (EC 3.4.22.-) ; Caspase 8 (EC 3.4.22.-)
Language	English
Publishing date	2021-04-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-87155-5
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