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Article ; Online: AP4 induces JNK1 and a miR-22-3p/FOSL1 feed-forward loop to activate AP-1 and promote colorectal cancer metastasis.

Chou, Jinjiang / Kaller, Markus / Rokavec, Matjaz / Liu, Fangteng / Hermeking, Heiko

Cancer communications (London, England)

2024 Volume 44, Issue 3, Page(s) 433–437

MeSH term(s)	Humans ; Transcription Factor AP-1 ; MicroRNAs/genetics ; Colorectal Neoplasms/pathology
Chemical Substances	Transcription Factor AP-1 ; MicroRNAs ; MIRN22 microRNA, human
Language	English
Publishing date	2024-01-15
Publishing country	United States
Document type	Letter
ISSN	2523-3548
ISSN (online)	2523-3548
DOI	10.1002/cac2.12514
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Book ; Online ; Thesis: Characterization of miR-34 effectors in colorectal cancer

Huang, Zekai [Verfasser] / Hermeking, Heiko [Akademischer Betreuer]

2024

Author's details	Zekai Huang ; Betreuer: Heiko Hermeking
Keywords	Medizin, Gesundheit ; Medicine, Health
Subject code	sg610
Language	English
Publisher	Universitätsbibliothek der Ludwig-Maximilians-Universität
Publishing place	München
Document type	Book ; Online ; Thesis
Database	Digital theses on the web

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Article ; Online: Squalene epoxidase/SQLE is a candidate target for treatment of colorectal cancers with

Du, Yuyun / Rokavec, Matjaz / Hermeking, Heiko

International journal of biological sciences

2023 Volume 19, Issue 13, Page(s) 4103–4122

Abstract: Elevated expression of c-MYC and inactivation ... ...

Abstract	Elevated expression of c-MYC and inactivation of
MeSH term(s)	Humans ; Squalene Monooxygenase/genetics ; Tumor Suppressor Protein p53/genetics ; Mutation ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Cholesterol
Chemical Substances	Squalene Monooxygenase (EC 1.14.14.17) ; Tumor Suppressor Protein p53 ; Cholesterol (97C5T2UQ7J)
Language	English
Publishing date	2023-08-06
Publishing country	Australia
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2179208-2
ISSN	1449-2288 ; 1449-2288
ISSN (online)	1449-2288
ISSN	1449-2288
DOI	10.7150/ijbs.85724
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Article: c-MYC-Induced AP4 Attenuates DREAM-Mediated Repression by p53.

Kaller, Markus / Shi, Wenjing / Hermeking, Heiko

Cancers

2023 Volume 15, Issue 4

Abstract: Background: The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor ... ...

Abstract	Background: The deregulated expression of the c-MYC oncogene activates p53, which is presumably mediated by ARF/INK4, as well as replication-stress-induced DNA damage. Here, we aimed to determine whether the c-MYC-inducible AP4 transcription factor plays a role in this context using a genetic approach. Methods: We used a CRISPR/Cas9 approach to generate Results: Loss of Conclusions: Our results establish AP4 as a pivotal factor at the crossroads of c-MYC, E2F, and p53 target gene regulation.
Language	English
Publishing date	2023-02-11
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041162
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Article: Nidogen-1/NID1 Function and Regulation during Progression and Metastasis of Colorectal Cancer.

Rokavec, Matjaz / Jaeckel, Stephanie / Hermeking, Heiko

Cancers

2023 Volume 15, Issue 22

Abstract: We have previously shown that the extracellular matrix and basement membrane protein Nidogen1 (NID1) is secreted by more malignant, mesenchymal-like CRC cells and induces the epithelial-mesenchymal transition (EMT) and promotes the migration and invasion ...

Abstract	We have previously shown that the extracellular matrix and basement membrane protein Nidogen1 (NID1) is secreted by more malignant, mesenchymal-like CRC cells and induces the epithelial-mesenchymal transition (EMT) and promotes the migration and invasion of less malignant, epithelial-like CRC cells. Here, we performed a comprehensive bioinformatics analysis of multiple datasets derived from CRC patients and showed that elevated expression of
Language	English
Publishing date	2023-11-07
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15225316
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Article ; Online: Development and Validation of a 15-gene Expression Signature with Superior Prognostic Ability in Stage II Colorectal Cancer.

Rokavec, Matjaz / Özcan, Elif / Neumann, Jens / Hermeking, Heiko

Cancer research communications

2023 Volume 3, Issue 8, Page(s) 1689–1700

Abstract: Currently, there is no consensus about the use of adjuvant chemotherapy for patients with stage II colorectal cancer. Here, we aimed to identify and validate a prognostic mRNA expression signature for the stratification of patients with stage II ... ...

Abstract	Currently, there is no consensus about the use of adjuvant chemotherapy for patients with stage II colorectal cancer. Here, we aimed to identify and validate a prognostic mRNA expression signature for the stratification of patients with stage II colorectal cancer according to their risk for relapse. First, publicly available mRNA expression profiling datasets from 792 primary, stage II colorectal cancers from six different training cohorts were analyzed to identify genes that are consistently associated with patient relapse-free survival (RFS). Second, the identified gene expression signature was experimentally validated using NanoString technology and computationally refined on primary colorectal cancer samples from 205 patients with stage II colorectal cancer. Third, the refined signature was validated in two independent publicly available cohorts of 166 patients with stage II colorectal cancer. Bioinformatics analysis of training cohorts identified a 61-gene signature that was highly significantly associated with RFS (HR = 37.08, Significance: We identified and validated a 15-gene expression signature for robust prognostication and stratification of patients with stage II colorectal cancer, with superior performance when compared with currently used biomarkers. Therefore, the 15-gene expression signature has the potential to improve the prognostication and treatment decisions for patients with stage II colorectal cancer.
MeSH term(s)	Humans ; Prognosis ; Transcriptome/genetics ; Colorectal Neoplasms/genetics ; RNA, Messenger
Chemical Substances	RNA, Messenger
Language	English
Publishing date	2023-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2767-9764
ISSN (online)	2767-9764
DOI	10.1158/2767-9764.CRC-22-0489
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Article ; Online: Salicylate induces AMPK and inhibits c-MYC to activate a NRF2/ARE/miR-34a/b/c cascade resulting in suppression of colorectal cancer metastasis.

Liu, Chunfeng / Rokavec, Matjaz / Huang, Zekai / Hermeking, Heiko

Cell death & disease

2023 Volume 14, Issue 10, Page(s) 707

Abstract: Aspirin and its active metabolite salicylate have emerged as promising agents for the chemoprevention of colorectal cancer (CRC). Moreover, aspirin suppresses the progression of established CRCs. However, the underlying molecular mechanisms are not ... ...

Abstract	Aspirin and its active metabolite salicylate have emerged as promising agents for the chemoprevention of colorectal cancer (CRC). Moreover, aspirin suppresses the progression of established CRCs. However, the underlying molecular mechanisms are not completely understood. Here we found that salicylate induces the expression of the miR-34a and miR-34b/c genes, which encode tumor suppressive microRNAs, in a p53-independent manner. Salicylate activated AMPK, thereby activating NRF2, which directly induced miR-34a/b/c expression via ARE motifs. In addition, salicylate suppressed c-MYC, a known repressor of NRF2-mediated transactivation, via activating AMPK. The suppression of c-MYC by salicylate was necessary for NRF2-mediated activation of miR-34a/b/c. Inactivation of miR-34a/b/c largely abrogated the inhibitory effects of salicylate on migration, invasion and metastasis formation by CRC cells. In the future, aspirin and its derivates may be used therapeutically to activate miR-34a and miR-34b/c in tumors that have lost p53.
MeSH term(s)	Humans ; AMP-Activated Protein Kinases/metabolism ; NF-E2-Related Factor 2/genetics ; NF-E2-Related Factor 2/metabolism ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Salicylates/pharmacology ; Cell Line, Tumor ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Aspirin/pharmacology ; Gene Expression Regulation, Neoplastic
Chemical Substances	AMP-Activated Protein Kinases (EC 2.7.11.31) ; NF-E2-Related Factor 2 ; Tumor Suppressor Protein p53 ; Salicylates ; MicroRNAs ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2023-10-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06226-9
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Article ; Online: CRISPR/Cas9-mediated inactivation of miR-34a and miR-34b/c in HCT116 colorectal cancer cells: comprehensive characterization after exposure to 5-FU reveals EMT and autophagy as key processes regulated by miR-34.

Huang, Zekai / Kaller, Markus / Hermeking, Heiko

Cell death and differentiation

2023 Volume 30, Issue 8, Page(s) 2017–2034

Abstract: The miR-34a and miR-34b/c encoding genes represent direct targets of the p53 transcription factor, and presumably mediate part of the tumor suppressive effects of p53. Here, we sought to determine their functional relevance by inactivating miR-34a and/or ...

Abstract	The miR-34a and miR-34b/c encoding genes represent direct targets of the p53 transcription factor, and presumably mediate part of the tumor suppressive effects of p53. Here, we sought to determine their functional relevance by inactivating miR-34a and/or miR-34b/c using a CRISPR/Cas9 approach in the colorectal cancer (CRC) cell line HCT116. Concomitant deletion of miR-34a and miR-34b/c resulted in significantly reduced suppression of proliferation after p53 activation, enhanced migration, invasion and EMT, as well as reduced sensitivity to chemotherapeutics, increased stress-induced autophagic flux, decreased apoptosis and upregulation of autophagy-related genes after 5-FU treatment. However, inactivation of singular miR-34a or miR-34b/c had little effects on the aforementioned processes. RNA-Seq analysis revealed that concomitant deletion of miR-34a/b/c caused EMT signature enrichment, impaired gene repression by the p53-DREAM pathway and elevated autophagy after 5-FU treatment. A gene signature comprised of mRNAs significantly upregulated after combined inactivation of miR-34a and miR-34b/c showed a significant association with the invasive colon cancer subtype CMS4 and poor overall survival in two CRC patient cohorts, and with 5-FU resistance in CRC cell lines. In miR-34a/b/c-deficient cells the upregulated miR-34 target FOXM1 directly induced p62 and ATG9A, which increased autophagy and consequently attenuated apoptosis and rendered the miR-34a/b/c-KO cells more resistant to 5-FU. Inhibition of autophagy by depletion of ATG9A or chloroquine re-sensitized miR-34a/b/c-deficient HCT116 cells to 5-FU. In summary, our findings show a complementary role of miR-34a and miR-34b/c in the regulation of EMT and autophagy which may be relevant for CRC therapy in the future.
MeSH term(s)	Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; HCT116 Cells ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; CRISPR-Cas Systems/genetics ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Fluorouracil/pharmacology ; Autophagy/genetics ; Gene Expression Regulation, Neoplastic
Chemical Substances	MicroRNAs ; Tumor Suppressor Protein p53 ; Fluorouracil (U3P01618RT) ; MIRN34 microRNA, human
Language	English
Publishing date	2023-07-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-023-01193-2
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Zs.A 4230: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Curcumin activates a ROS/KEAP1/NRF2/miR-34a/b/c cascade to suppress colorectal cancer metastasis.

Liu, Chunfeng / Rokavec, Matjaz / Huang, Zekai / Hermeking, Heiko

Cell death and differentiation

2023 Volume 30, Issue 7, Page(s) 1771–1785

Abstract: Curcumin, a natural phytochemical isolated from tumeric roots, represents a candidate for prevention and therapy of colorectal cancer/CRC. However, the exact mechanism of action and the downstream mediators of curcumin's tumor suppressive effects have ... ...

Abstract	Curcumin, a natural phytochemical isolated from tumeric roots, represents a candidate for prevention and therapy of colorectal cancer/CRC. However, the exact mechanism of action and the downstream mediators of curcumin's tumor suppressive effects have remained largely unknown. Here we used a genetic approach to determine the role of the p53/miR-34 pathway as mediator of the effects of curcumin. Three isogenic CRC cell lines rendered deficient for the p53, miR-34a and/or miR-34b/c genes were exposed to curcumin and subjected to cell biological analyses. siRNA-mediated inhibition and ectopic expression of NRF2, as well as Western blot, qPCR and qChIP analyses of its target genes were performed. CRC cells were i.v. injected into NOD/SCID mice and lung-metastases formation was determined by longitudinal, non-invasive imaging. In CRC cells curcumin induced apoptosis and senescence, and suppressed migration and invasion in a p53-independent manner. Curcumin activated the KEAP1/NRF2/ARE pathway by inducing ROS. Notably, curcumin induced miR-34a and miR-34b/c expression in a ROS/NRF2-dependent and p53-independent manner. NRF2 directly induced miR-34a and miR-34b/c via occupying multiple ARE motifs in their promoter regions. Curcumin reverted repression of miR-34a and miR-34b/c induced by IL6 and hypoxia. Deletion of miR-34a and miR-34b/c significantly reduced curcumin-induced apoptosis and senescence, and prevented the inhibition of migration and invasion by curcumin or ectopic NRF2. In CRC cells curcumin induced MET and prevented the formation of lung-metastases in mice in a miR-34a-dependent manner. In addition, we found that curcumin may enhance the therapeutic effects of 5-FU on CRC cells deficient for p53 and miR-34a/b/c. Activation of the KEAP1/NRF2/miR-34a/b/c axis mediates the tumor suppressive activity of curcumin and suggests a new approach for activating miR-34 genes in tumors for therapeutic purposes.
MeSH term(s)	Animals ; Mice ; Cell Line, Tumor ; Colorectal Neoplasms/metabolism ; Colorectal Neoplasms/therapy ; Curcumin/pharmacology ; Gene Expression Regulation, Neoplastic ; Kelch-Like ECH-Associated Protein 1/metabolism ; Lung Neoplasms/secondary ; Lung Neoplasms/therapy ; Mice, Inbred NOD ; Mice, SCID ; MicroRNAs ; NF-E2-Related Factor 2/metabolism ; Reactive Oxygen Species/metabolism ; Tumor Suppressor Protein p53/metabolism
Chemical Substances	Curcumin (IT942ZTH98) ; Kelch-Like ECH-Associated Protein 1 ; MicroRNAs ; NF-E2-Related Factor 2 ; Reactive Oxygen Species ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-05-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1225672-9
ISSN	1476-5403 ; 1350-9047
ISSN (online)	1476-5403
ISSN	1350-9047
DOI	10.1038/s41418-023-01178-1
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Article: miR-34a and IRE1A/XBP-1(S) Form a Double-Negative Feedback Loop to Regulate Hypoxia-Induced EMT, Metastasis, Chemo-Resistance and Autophagy.

Bouznad, Nassim / Rokavec, Matjaz / Öner, Meryem Gülfem / Hermeking, Heiko

Cancers

2023 Volume 15, Issue 4

Abstract: Tumor-associated hypoxia, i.e., decreased availability of oxygen, results in a poor clinical outcome since it promotes EMT, metastasis, and chemotherapy-resistance. We have previously identified p53 and its target miR-34a, as critical determinants of the ...

Abstract	Tumor-associated hypoxia, i.e., decreased availability of oxygen, results in a poor clinical outcome since it promotes EMT, metastasis, and chemotherapy-resistance. We have previously identified p53 and its target miR-34a, as critical determinants of the effect of hypoxia on colorectal cancer (CRC). Here, we aimed to characterize mechanisms that contribute to the selective advantage of cells with loss of p53/miR-34a function in a hypoxic environment. Using in silico prediction, we identified XBP-1 and IRE1A as potential miR-34a targets. IRE1A and XBP-1 are central components of the unfolded protein response that is activated by ER stress, which is also induced in tumor cells as a response to harsh conditions surrounding tumors such as hypoxia and a limited supply of nutrients. Here we characterized the XBP-1(S) transcription factor and its regulator IRE1A as direct, conserved miR-34a targets in CRC cells. After hypoxia and DNA damage, IRE1A and XBP-1 were repressed by p53 in a miR-34a-dependent manner, whereas
Language	English
Publishing date	2023-02-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers15041143
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