scholarly journals Reciprocal Regulation among miR-181d/CRY2/FBXL3/c-myc Signaling Axis Modulates Metabolism in Colorectal Cancer

RNA & DISEASE ◽  
2018 ◽  
Vol 5 ◽  
Keyword(s):  
Colorectal Cancer ◽  
Reciprocal Regulation ◽  
Signaling Axis

Role of Regulatory Oncogenic or Tumor Suppressor miRNAs of PI3K/AKT Signaling Axis in the Pathogenesis of Colorectal Cancer

2019 ◽  
Vol 24 (39) ◽  
pp. 4605-4610 ◽  
Author(s):  
Atena Soleimani ◽  
Farzad Rahmani ◽  
Gordon A. Ferns ◽  
Mikhail Ryzhikov ◽  
Amir Avan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Current Knowledge ◽  
Akt Signaling ◽  
Tumor Tissues ◽  
Radio Therapy ◽  
Signaling Axis ◽  
Cancer Tumor ◽  
Novel Biomarkers

Colorectal cancer (CRC) is the leading cause of cancer death worldwide and its incidence is increasing. In most patients with CRC, the PI3K/AKT signaling axis is over-activated. Regulatory oncogenic or tumor suppressor microRNAs (miRNAs) for PI3K/AKT signaling regulate cell proliferation, migration, invasion, angiogenesis, as well as resistance to chemo-/radio-therapy in colorectal cancer tumor tissues. Thus, regulatory miRNAs of PI3K/AKT/mTOR signaling represent novel biomarkers for new patient diagnosis and obtaining clinically invaluable information from post-treatment CRC patients for improving therapeutic strategies. This review summarizes the current knowledge of miRNAs’ regulatory roles of PI3K/AKT signaling in CRC pathogenesis.

scholarly journals Metformin and Niclosamide Synergistically Suppress Wnt and YAP in APC-Mutated Colorectal Cancer

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3437
Author(s):  
Hee Eun Kang ◽  
Yoojeong Seo ◽  
Jun Seop Yun ◽  
Sang Hyun Song ◽  
Dawool Han ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cancer Progression ◽  
Therapeutic Strategy ◽  
Target Gene ◽  
Advanced Colorectal Cancer ◽  
Therapeutic Potential ◽  
Cancer Stemness ◽  
Reciprocal Regulation ◽  
Canonical Wnt

The Wnt and Hippo pathways are tightly coordinated and understanding their reciprocal regulation may provide a novel therapeutic strategy for cancer. Anti-helminthic niclosamide is an effective inhibitor of Wnt and is now in a phase II trial for advanced colorectal cancer (CRC) patients. We found that Axin2, an authentic target gene of canonical Wnt, acts as aYAP phosphorylation activator in APC-mutated CRC. While niclosamide effectively suppresses Wnt, it also inhibits Hippo, limiting its therapeutic potential for CRC. To overcome this limitation, we utilized metformin, a clinically available AMPK activator. This combinatory approach not only suppresses canonical Wnt activity, but also inhibits YAP activity in CRC cancer cells and in patient-derived cancer organoid through the suppression of cancer stemness. Further, combinatory oral administration suppressed in vivo tumorigenesis and the cancer progression of APC-MIN mice models. Our observations provide not only a reciprocal link between Wnt and Hippo, but also clinically available novel therapeutics that are able to target Wnt and YAP in APC-mutated CRC.

scholarly journals EphA2 and EGFR: Friends in Life, Partners in Crime. Can EphA2 Be a Predictive Biomarker of Response to Anti-EGFR Agents?

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 700
Author(s):  
Mario Cioce ◽  
Vito Michele Fazio
Keyword(s):  
Colorectal Cancer ◽  
Solid Tumors ◽  
Receptor Tyrosine Kinase ◽  
Predictive Biomarker ◽  
Eph Receptors ◽  
Oncogenic Signaling ◽  
Induced Stress ◽  
Molecular Determinants ◽  
Signaling Axis ◽  
Context Specific

The Eph receptors represent the largest group among Receptor Tyrosine kinase (RTK) families. The Eph/ephrin signaling axis plays center stage during development, and the deep perturbation of signaling consequent to its dysregulation in cancer reveals the multiplicity and complexity underlying its function. In the last decades, they have emerged as key players in solid tumors, including colorectal cancer (CRC); however, what causes EphA2 to switch between tumor-suppressive and tumor-promoting function is still an active theater of investigation. This review summarizes the recent advances in understanding EphA2 function in cancer, with detail on the molecular determinants of the oncogene-tumor suppressor switch function of EphA2. We describe tumor context-specific examples of EphA2 signaling and the emerging role EphA2 plays in supporting cancer—stem—cell-like populations and overcoming therapy-induced stress. In such a frame, we detail the interaction of the EphA2 and EGFR pathway in solid tumors, including colorectal cancer. We discuss the contribution of the EphA2 oncogenic signaling to the resistance to EGFR blocking agents, including cetuximab and TKIs.

GRIM‐19 repressed hypoxia‐induced invasion and EMT of colorectal cancer by repressing autophagy through inactivation of STAT3/HIF‐1α signaling axis

2018 ◽  
Vol 234 (8) ◽  
pp. 12800-12808 ◽  
Author(s):  
Juan Zhang ◽  
Dake Chu ◽  
Takuji Kawamura ◽  
Kiyohito Tanaka ◽  
Shuixiang He
Keyword(s):  
Colorectal Cancer ◽  
Signaling Axis

scholarly journals Reciprocal regulation of BMF and BIRC5 (Survivin) linked to Eomes overexpression in colorectal cancer

2016 ◽  
Vol 381 (2) ◽  
pp. 341-348 ◽  
Author(s):  
Rong Wang ◽  
Yuki Kang ◽  
Christiane V. Löhr ◽  
Kay A. Fischer ◽  
C. Samuel Bradford ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Reciprocal Regulation

scholarly journals TRPC1 promotes the genesis and progression of colorectal cancer via activating CaM-mediated PI3K/AKT signaling axis

Oncogenesis ◽  
2021 ◽  
Vol 10 (10) ◽  
Author(s):  
Yang Sun ◽  
Chen Ye ◽  
Wen Tian ◽  
Wen Ye ◽  
Yuan-Yuan Gao ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Cycle ◽  
Tumor Growth ◽  
Cell Cycle Progression ◽  
Akt Signaling ◽  
Cycle Progression ◽  
Colorectal Tumorigenesis ◽  
Signaling Axis

AbstractTransient receptor potential canonical (TRPC) channels are the most prominent nonselective cation channels involved in various diseases. However, the function, clinical significance, and molecular mechanism of TRPCs in colorectal cancer (CRC) progression remain unclear. In this study, we identified that TRPC1 was the major variant gene of the TRPC family in CRC patients. TRPC1 was upregulated in CRC tissues compared with adjacent normal tissues and high expression of TRPC1 was associated with more aggressive tumor progression and poor overall survival. TRPC1 knockdown inhibited cell proliferation, cell-cycle progression, invasion, and migration in vitro, as well as tumor growth in vivo; whereas TRPC1 overexpression promoted colorectal tumor growth and metastasis in vitro and in vivo. In addition, colorectal tumorigenesis was significantly attenuated in Trpc1-/- mice. Mechanistically, TRPC1 could enhance the interaction between calmodulin (CaM) and the PI3K p85 subunit by directly binding to CaM, which further activated the PI3K/AKT and its downstream signaling molecules implicated in cell cycle progression and epithelial-mesenchymal transition. Silencing of CaM attenuated the oncogenic effects of TRPC1. Taken together, these results provide evidence that TRPC1 plays a pivotal oncogenic role in colorectal tumorigenesis and tumor progression by activating CaM-mediated PI3K/AKT signaling axis. Targeting TRPC1 represents a novel and specific approach for CRC treatment.

scholarly journals Novel Epigenetic CREB-miR-630 Signaling Axis Regulates Radiosensitivity in Colorectal Cancer

PLoS ONE ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. e0133870 ◽  
Author(s):  
Yan Zhang ◽  
Jiang Yu ◽  
Hao Liu ◽  
Wenhui Ma ◽  
Li Yan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Signaling Axis
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