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Article ; Online: Nickel-Catalyzed Domino Reaction of α-Aryloxyacetonitriles with Arylboronic Acids: Synthesis of 2-Aroylbenzo[

Subramaniam, Subhashini V / Dharmalingam, Vijaya Kumaran / Bhattacharya, Anwesha / Peruncheralathan, Saravanan

Organic letters

2023 Volume 25, Issue 46, Page(s) 8225–8229

Abstract: We disclose the first catalytic domino reaction of α-(2-formylaryloxy)acetonitriles with arylboronic acids, yielding a range of 2-aroylbenzo[ ...

Abstract	We disclose the first catalytic domino reaction of α-(2-formylaryloxy)acetonitriles with arylboronic acids, yielding a range of 2-aroylbenzo[
Language	English
Publishing date	2023-11-14
Publishing country	United States
Document type	Journal Article
ISSN	1523-7052
ISSN (online)	1523-7052
DOI	10.1021/acs.orglett.3c03241
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Article ; Online: Targeting Major Signaling Pathways of Bladder Cancer with Phytochemicals: A Review.

Chestnut, Connor / Subramaniam, Dharmalingam / Dandawate, Prasad / Padhye, Subhash / Taylor, John / Weir, Scott / Anant, Shrikant

Nutrition and cancer

2020 Volume 73, Issue 11-12, Page(s) 2249–2271

Abstract: Bladder cancer is the ... ...

Abstract	Bladder cancer is the 9
MeSH term(s)	Genistein ; Humans ; Phosphatidylinositol 3-Kinases ; Phytochemicals/pharmacology ; Phytochemicals/therapeutic use ; Signal Transduction ; Urinary Bladder Neoplasms/drug therapy
Chemical Substances	Phytochemicals ; Genistein (DH2M523P0H)
Language	English
Publishing date	2020-12-11
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	424433-3
ISSN	1532-7914 ; 0163-5581
ISSN (online)	1532-7914
ISSN	0163-5581
DOI	10.1080/01635581.2020.1856895
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Article: Targeting Major Signaling Pathways of Bladder Cancer with Phytochemicals: A Review

Chestnut, Connor / Subramaniam, Dharmalingam / Dandawate, Prasad / Padhye, Subhash / Taylor, John / Weir, Scott / Anant, Shrikant

Nutrition and cancer. 2021 Dec. 31, v. 73, no. 11-12

2021

Abstract: Bladder cancer is the 9ᵗʰ most prevalent cancer worldwide and carries a protracted treatment course with significant patient expense, morbidity, and mortality. Over 95% of bladder cancers arise from the urothelium and invade into the underlying muscle ... ...

Abstract	Bladder cancer is the 9ᵗʰ most prevalent cancer worldwide and carries a protracted treatment course with significant patient expense, morbidity, and mortality. Over 95% of bladder cancers arise from the urothelium and invade into the underlying muscle layer before metastasizing. Trans-urethral resection and BCG therapy is the current first-line treatment for non-muscle invasive bladder cancer but carries a high rate of tumor recurrence and progression. The poor outcomes associated with advanced disease indicate the urgent need for new and improved treatment strategies. There is increasing investigation into the molecular signaling pathways involved in bladder cancer pathogenesis with the goal of uncovering potential therapeutic targets. This article reviews the major signaling pathways implicated in bladder cancer, including PI3K/AKT/mTOR, Ras/Raf/MEK/MAPK, NF-κB, Wnt/β‐catenin, Notch, Hedgehog, Hippo, JAK/STAT, and TGF-β as well as major cellular receptors central to cancer pathophysiology, including EGFR, Her2, FGFR, and VEGF. We also discuss various naturally occurring phytochemicals that show evidence of targeting these molecular pathways including curcumin, resveratrol, green tea polyphenols, sulforaphane, erucin, genistein, genipin, baicalein, quercetin, isoquercitin, vitamin E, parthenolide, dioscin, triptolide, kaempferol, pterostilbene, isoliquiritigenin, and escin. This review highlights the potential use of these compounds in treatment of bladder cancer.
Keywords	Erinaceidae ; bladder ; curcumin ; genistein ; green tea ; kaempferol ; morbidity ; mortality ; muscles ; nutrition ; pathogenesis ; pathophysiology ; patients ; polyphenols ; pterostilbene ; quercetin ; resection ; resveratrol ; sulforaphane ; urinary bladder neoplasms ; vitamin E
Language	English
Dates of publication	2021-1231
Size	p. 2249-2271.
Publishing place	Taylor & Francis
Document type	Article
ZDB-ID	424433-3
ISSN	1532-7914 ; 0163-5581
ISSN (online)	1532-7914
ISSN	0163-5581
DOI	10.1080/01635581.2020.1856895
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Article ; Online: Editor's Note: Diphenyl Difluoroketone: A Curcumin Derivative with Potent In Vivo Anticancer Activity.

Subramaniam, Dharmalingam / May, Randal / Sureban, Sripathi M / Lee, Katherine B / George, Robert / Kuppusamy, Periannan / Ramanujam, Rama P / Hideg, Kalman / Dieckgraefe, Brian K / Houchen, Courtney W / Anant, Shrikant

Cancer research

2022 Volume 82, Issue 16, Page(s) 2951

Language	English
Publishing date	2022-08-15
Publishing country	United States
Document type	Published Erratum
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-22-1949
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Article ; Online: 3508 Ciclopirox Olamine Demonstrates Inhibitory Effects on Esophageal Tumor Cells

Randi Ryan / Shrikant Anant / Prabhu Ramamoorthy / Dharmalingam Subramaniam / Scott Weir

Journal of Clinical and Translational Science, Vol 3, Pp 5-

2019 Volume 5

Abstract: OBJECTIVES/SPECIFIC AIMS: Drug repositioning has the potential to accelerate translation of novel cancer chemotherapeutics from bench to bedside. The goal of this study was to determine the effects of ciclopirox olamine (CPX) on esophageal tumor cells. ... ...

Abstract	OBJECTIVES/SPECIFIC AIMS: Drug repositioning has the potential to accelerate translation of novel cancer chemotherapeutics from bench to bedside. The goal of this study was to determine the effects of ciclopirox olamine (CPX) on esophageal tumor cells. METHODS/STUDY POPULATION: We tested the effect of CPX on four esophageal cancer cell lines, assessing cell proliferation and viability by hexosaminidase and clonogenicity assay, respectively. We analyzed the effects of CPX on three-dimensional (3D) esophageal tumor cell spheroids. We also analyzed effects on cell cycle by flow cytometry. For mechanism, we performed western blots for proteins involved in cell cycle regulation, apoptosis and the Wnt/β-catenin pathway. For in vivo effects, we performed a murine xenograft model with intraperitoneal administration of CPX (100 mg/Kg body weight daily). RESULTS/ANTICIPATED RESULTS: CPX inhibited growth of all cell lines in a time and concentration-dependent manner. CPX also inhibited growth of esophageal spheroids. Cell cycle analysis demonstrated G0/G1 arrest in cells treated with CPX. Western blot analyses demonstrated decreased expression of cyclinD1, CDK4, CDK6, and transcriptionally active β-catenin, supporting the role of CPX in cell cycle inhibition and decreased β-catenin activity. Finally, treatment of nude mice with CPX significantly decreased tumor xenograft volume. DISCUSSION/SIGNIFICANCE OF IMPACT: CPX demonstrates anti-tumor properties in esophageal cancer cell lines. The current results justify further research into the mechanism of this inhibition. Additionally, given its established safety in humans, CPX is a potential candidate for repositioning as an adjunct treatment for esophageal cancer.
Keywords	Medicine ; R
Language	English
Publishing date	2019-03-01T00:00:00Z
Publisher	Cambridge University Press
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Targeting Cancer Stem Cells for Chemoprevention of Pancreatic Cancer.

Subramaniam, Dharmalingam / Kaushik, Gaurav / Dandawate, Prasad / Anant, Shrikant

Current medicinal chemistry

2017 Volume 25, Issue 22, Page(s) 2585–2594

Abstract: Pancreatic ductal adenocarcinoma is one of the deadliest cancers worldwide and the fourth leading cause of cancer-related deaths in United States. Regardless of the advances in molecular pathogenesis and consequential efforts to suppress the disease, ... ...

Abstract	Pancreatic ductal adenocarcinoma is one of the deadliest cancers worldwide and the fourth leading cause of cancer-related deaths in United States. Regardless of the advances in molecular pathogenesis and consequential efforts to suppress the disease, this cancer remains a major health problem in United States. By 2030, the projection is that pancreatic cancer will be climb up to be the second leading cause of cancer-related deaths in the United States. Pancreatic cancer is a rapidly invasive and highly metastatic cancer, and does not respond to standard therapies. Emerging evidence supports that the presence of a unique population of cells called cancer stem cells (CSCs) as potential cancer inducing cells and efforts are underway to develop therapeutic strategies targeting these cells. CSCs are rare quiescent cells, and with the capacity to self-renew through asymmetric/symmetric cell division, as well as differentiate into various lineages of cells in the cancer. Studies have been shown that CSCs are highly resistant to standard therapy and also responsible for drug resistance, cancer recurrence and metastasis. To overcome this problem, we need novel preventive agents that target these CSCs. Natural compounds or phytochemicals have ability to target these CSCs and their signaling pathways. Therefore, in the present review article, we summarize our current understanding of pancreatic CSCs and their signaling pathways, and the phytochemicals that target these cells including curcumin, resveratrol, tea polyphenol EGCG (epigallocatechin- 3-gallate), crocetinic acid, sulforaphane, genistein, indole-3-carbinol, vitamin E δ- tocotrienol, Plumbagin, quercetin, triptolide, Licofelene and Quinomycin. These natural compounds or phytochemicals, which inhibit cancer stem cells may prove to be promising agents for the prevention and treatment of pancreatic cancers.
MeSH term(s)	Catechin/analogs & derivatives ; Catechin/pharmacology ; Catechin/therapeutic use ; Hedgehog Proteins/antagonists & inhibitors ; Hedgehog Proteins/metabolism ; Humans ; Intracellular Signaling Peptides and Proteins/antagonists & inhibitors ; Intracellular Signaling Peptides and Proteins/metabolism ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Mitogen-Activated Protein Kinases/metabolism ; Neoplastic Stem Cells/cytology ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/prevention & control ; Phytochemicals/pharmacology ; Phytochemicals/therapeutic use ; Protein-Serine-Threonine Kinases/antagonists & inhibitors ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction/drug effects ; Wnt Proteins/antagonists & inhibitors ; Wnt Proteins/metabolism
Chemical Substances	Hedgehog Proteins ; Intracellular Signaling Peptides and Proteins ; Phytochemicals ; Wnt Proteins ; Catechin (8R1V1STN48) ; epigallocatechin gallate (BQM438CTEL) ; DCLK1 protein, human (EC 2.7.1.11) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2017-01-30
Publishing country	United Arab Emirates
Document type	Journal Article ; Review
ZDB-ID	1319315-6
ISSN	1875-533X ; 0929-8673
ISSN (online)	1875-533X
ISSN	0929-8673
DOI	10.2174/0929867324666170127095832
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Article ; Online: Honokiol Affects Stem Cell Viability by Suppressing Oncogenic YAP1 Function to Inhibit Colon Tumorigenesis

Dharmalingam Subramaniam / Sivapriya Ponnurangam / Satish Ramalingam / Deep Kwatra / Prasad Dandawate / Scott J. Weir / Shahid Umar / Roy A. Jensen / Shrikant Anant

Cells, Vol 10, Iss 1607, p

2021 Volume 1607

Abstract: Honokiol (HNK) is a biphenolic compound that has been used in traditional medicine for treating various ailments, including cancers. In this study, we determined the effect of HNK on colon cancer cells in culture and in a colitis-associated cancer model. ...

Abstract	Honokiol (HNK) is a biphenolic compound that has been used in traditional medicine for treating various ailments, including cancers. In this study, we determined the effect of HNK on colon cancer cells in culture and in a colitis-associated cancer model. HNK treatment inhibited proliferation and colony formation while inducing apoptosis. In addition, HNK suppressed colonosphere formation. Molecular docking suggests that HNK interacts with reserve stem cell marker protein DCLK1, with a binding energy of −7.0 Kcal/mol. In vitro kinase assays demonstrated that HNK suppressed the DCLK1 kinase activity. HNK also suppressed the expression of additional cancer stem cell marker proteins LGR5 and CD44. The Hippo signaling pathway is active in intestinal stem cells. In the canonical pathway, YAP1 is phosphorylated at Ser127 by upstream Mst1/2 and Lats1/2. This results in the sequestration of YAP1 in the cytoplasm, thereby not allowing YAP1 to translocate to the nucleus and interact with TEAD1-4 transcription factors to induce gene expression. However, HNK suppressed Ser127 phosphorylation in YAP1, but the protein remains sequestered in the cytoplasm. We further determined that this occurs by YAP1 interacting with PUMA. To determine if this also occurs in vivo, we performed studies in an AOM/DSS induced colitis-associated cancer model. HNK administered by oral gavage at a dose of 5mg/kg bw for 24 weeks demonstrated a significant reduction in the expression of YAP1 and TEAD1 and in the stem marker proteins. Together, these data suggest that HNK prevents colon tumorigenesis in part by inducing PUMA-YAP1 interaction and cytoplasmic sequestration, thereby suppressing the oncogenic YAP1 activity.
Keywords	apoptosis ; cancer stem cells ; colonospheres ; spheroids ; colitis associated cancer ; hippo signaling ; Biology (General) ; QH301-705.5
Subject code	570
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Honokiol Affects Stem Cell Viability by Suppressing Oncogenic YAP1 Function to Inhibit Colon Tumorigenesis.

Subramaniam, Dharmalingam / Ponnurangam, Sivapriya / Ramalingam, Satish / Kwatra, Deep / Dandawate, Prasad / Weir, Scott J / Umar, Shahid / Jensen, Roy A / Anant, Shrikant

Cells

2021 Volume 10, Issue 7

Abstract	Honokiol (HNK) is a biphenolic compound that has been used in traditional medicine for treating various ailments, including cancers. In this study, we determined the effect of HNK on colon cancer cells in culture and in a colitis-associated cancer model. HNK treatment inhibited proliferation and colony formation while inducing apoptosis. In addition, HNK suppressed colonosphere formation. Molecular docking suggests that HNK interacts with reserve stem cell marker protein DCLK1, with a binding energy of -7.0 Kcal/mol. In vitro kinase assays demonstrated that HNK suppressed the DCLK1 kinase activity. HNK also suppressed the expression of additional cancer stem cell marker proteins LGR5 and CD44. The Hippo signaling pathway is active in intestinal stem cells. In the canonical pathway, YAP1 is phosphorylated at Ser127 by upstream Mst1/2 and Lats1/2. This results in the sequestration of YAP1 in the cytoplasm, thereby not allowing YAP1 to translocate to the nucleus and interact with TEAD1-4 transcription factors to induce gene expression. However, HNK suppressed Ser127 phosphorylation in YAP1, but the protein remains sequestered in the cytoplasm. We further determined that this occurs by YAP1 interacting with PUMA. To determine if this also occurs in vivo, we performed studies in an AOM/DSS induced colitis-associated cancer model. HNK administered by oral gavage at a dose of 5mg/kg bw for 24 weeks demonstrated a significant reduction in the expression of YAP1 and TEAD1 and in the stem marker proteins. Together, these data suggest that HNK prevents colon tumorigenesis in part by inducing PUMA-YAP1 interaction and cytoplasmic sequestration, thereby suppressing the oncogenic YAP1 activity.
MeSH term(s)	Adaptor Proteins, Signal Transducing/metabolism ; Animals ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/metabolism ; Biomarkers, Tumor/metabolism ; Biphenyl Compounds/pharmacology ; Carcinogenesis/drug effects ; Carcinogenesis/pathology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Colitis/complications ; Colonic Neoplasms/pathology ; Doublecortin-Like Kinases ; Down-Regulation/drug effects ; Hippo Signaling Pathway ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Lignans/pharmacology ; Male ; Mice, Inbred ICR ; Models, Biological ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/pathology ; Protein Binding/drug effects ; Protein Serine-Threonine Kinases/metabolism ; Proto-Oncogene Proteins/metabolism ; Signal Transduction/drug effects ; Transcription Factors/metabolism ; Tumor Stem Cell Assay ; YAP-Signaling Proteins ; Mice
Chemical Substances	Adaptor Proteins, Signal Transducing ; Apoptosis Regulatory Proteins ; BBC3 protein, human ; Biomarkers, Tumor ; Biphenyl Compounds ; Intracellular Signaling Peptides and Proteins ; Lignans ; Proto-Oncogene Proteins ; Transcription Factors ; YAP-Signaling Proteins ; YAP1 protein, human ; honokiol (11513CCO0N) ; DCLK1 protein, human (EC 2.7.1.11) ; Doublecortin-Like Kinases (EC 2.7.1.11) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-06-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10071607
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Article ; Online: A New Pentafluorothio-Substituted Curcuminoid with Superior Antitumor Activity.

Linder, Benedikt / Köhler, Leonhard H F / Reisbeck, Lisa / Menger, Dominic / Subramaniam, Dharmalingam / Herold-Mende, Christel / Anant, Shrikant / Schobert, Rainer / Biersack, Bernhard / Kögel, Donat

Biomolecules

2021 Volume 11, Issue 7

Abstract: A new and readily available pentafluorothiophenyl-substituted N-methyl-piperidone ... ...

Abstract	A new and readily available pentafluorothiophenyl-substituted N-methyl-piperidone curcuminoid
MeSH term(s)	Animals ; Animals, Genetically Modified ; Antineoplastic Agents, Phytogenic/chemical synthesis ; Antineoplastic Agents, Phytogenic/pharmacology ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; Curcumin/chemical synthesis ; Curcumin/pharmacology ; Diarylheptanoids/chemical synthesis ; Diarylheptanoids/pharmacology ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor/methods ; HCT116 Cells ; HT29 Cells ; Humans ; MCF-7 Cells ; Zebrafish
Chemical Substances	Antineoplastic Agents, Phytogenic ; Diarylheptanoids ; Curcumin (IT942ZTH98)
Language	English
Publishing date	2021-06-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom11070947
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Article: Manipulating miRNA Expression: A Novel Approach for Colon Cancer Prevention and Chemotherapy.

Ramalingam, Satish / Subramaniam, Dharmalingam / Anant, Shrikant

Current pharmacology reports

2015 Volume 1, Issue 3, Page(s) 141–153

Abstract: Small non-coding RNA has been implicated in the control of various cellular processes such as proliferation, apoptosis, and differentiation. About 50% of the miRNA genes are positioned in cancer-associated genomic regions. Several studies have shown that ...

Abstract	Small non-coding RNA has been implicated in the control of various cellular processes such as proliferation, apoptosis, and differentiation. About 50% of the miRNA genes are positioned in cancer-associated genomic regions. Several studies have shown that miRNA expression is deregulated in cancer and modulating their expression has reversed the cancer phenotype. Therefore, mechanisms to modulate microRNA (miRNA) activity have provided a novel opportunity for cancer prevention and therapy. In addition, a common cause for development of colorectal cancers is environmental and lifestyle factors. One such factor, diet has been shown to modulate miRNA expression in colorectal cancer patients. In this chapter, we will summarize the work demonstrating that miRNAs are novel promising drug targets for cancer chemoprevention and therapy. Improved delivery, increased stability and enhanced regulation of off-target effects will overcome the current challenges of this exciting approach in the field of cancer prevention and therapy.
Language	English
Publishing date	2015-05-06
Publishing country	Switzerland
Document type	Journal Article
ISSN	2198-641X
ISSN	2198-641X
DOI	10.1007/s40495-015-0020-3
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