Results 61 to 70 of about 33,936 (220)

Viability of human colorectal cancer cells HCT116, and other types of cancer cells or normal cells.

open access: yes, 2018
Viability of human colorectal cancer cells HCT116, and (B) other types of cancer cells or normal cells at fifth day from transfection with miR-8073 mimic or negative control sequence (miR-NC).
Aiko Takayama (6160544)   +4 more
core   +1 more source

Thioredoxin Reductase-1 as a Potential Biomarker in Fibroblast-Associated HCT116 Cancer Cell Progression and Dissemination in a Zebrafish Model

open access: yes, 2022
The tumor microenvironment, especially that of fibroblasts, strongly promotes colorectal cancer (CRC) progression. Progressive cancers usually accumulate high reactive oxygen species (ROS), leading to oxidative stress.
Tharathip Muangthong   +4 more
core   +1 more source

Artemether as a modulator of EMT in colorectal cancer: enhancing radiosensitivity and reversing chemo-radiation resistance

open access: yesBMC Gastroenterology
Background The efficacy of conventional chemoradiotherapy for colorectal cancer is often limited by resistance, with epithelial-mesenchymal transition being a key mechanism.
Lv Ge   +11 more
doaj   +1 more source

Swelling‐Programmed Topographical Guidance for Dynamic Spheroid Self‐Assembly via a Mechanochemical Hydrogel Niche

open access: yesAdvanced Functional Materials, EarlyView.
A swelling‐programmed micropatterned hydrogel guides adherent cells through a controlled transition from cell–matrix anchoring to cadherin‐mediated cell–cell compaction, enabling rapid assembly of high‐viability spheroids with defined size and morphology.
Han Gyeol Nam   +8 more
wiley   +1 more source

Growth inhibition and apoptosis in colorectal cancer cells induced by Vitamin D-Nanoemulsion (NVD): involvement of Wnt/β-catenin and other signal transduction pathways

open access: yesCell & Bioscience, 2019
Background More than the two decades, the question of whether vitamin D has a role in cancer frequency, development, and death has been premeditated in detail.
Suhail Razak   +4 more
doaj   +1 more source

Genetic variants in the calcium signaling pathway participate in the pathogenesis of colorectal cancer through the tumor microenvironment

open access: yesFrontiers in Oncology, 2023
BackgroundCancer risk is influenced by calcium signaling in intracellular and intercellular signaling pathways. However, the relationship between the calcium signaling pathway and colorectal cancer risk remains unknown.
Jing-Yu Wu   +5 more
doaj   +1 more source

Genome‐Wide In Vivo RNAi Screening Identifies HOXD4 as a Tumor Metastasis Suppressor in Colorectal Cancer

open access: yesAdvanced Science, EarlyView.
Metastasis remains a major challenge in colorectal cancer. Using an in vivo shRNA screening system, this study identifies Homeobox D4 as a key metastasis suppressor. Reduced Homeobox D4 expression is associated with aggressive tumor features. Functional and mechanistic analyses show that it inhibits epithelial‐mesenchymal transition by repressing ...
Zhi‐hua Ye   +9 more
wiley   +1 more source

The Transcriptomic and Genomic Analysis of Lamin A/C Expression in the Colon and in Colorectal Cancer [PDF]

open access: yes, 2011
Lamins A and C, also known as A-type lamins, are type V nuclear intermediate filament proteins which form an interlacing meshwork of filaments subjacent to the inner nuclear membrane termed the nuclear lamina.
RAHMAN-CASANS, SYED,FIDA,UR   +1 more
core  

Compound Bieshe Kang’ai inhibits proliferation and induces apoptosis in HCT116 human colorectal cancer cells

open access: yes, 2019
Purpose: To study the effect of Compound Bieshe Kang’ai (CBK) on proliferation and apoptosis in colorectal cancer cells.Methods: HCT116 colorectal cancer cells and FHs 74 Int intestinal cells were treated with CBK, followed by determination of cell ...
Lei, Nan   +10 more
core   +1 more source

Enhancing CAR‐T Cell Efficacy in Solid Tumors by Inhibiting CCL5/VEGF‐Mediated Angiogenesis

open access: yesAdvanced Science, EarlyView.
This study reveals that CAR‐T cells in solid tumors produce CCL5, which paradoxically induces VEGF and angiogenesis to promote tumor growth. Blocking CCL5/VEGF signaling—through gene knockout, or the CCR5 inhibitor maraviroc—significantly enhances the antitumor efficacy of CAR‑T therapy (the diagram was created in Biorender).
Shishuo Sun   +15 more
wiley   +1 more source

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