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Functional Molecules in Tracing and Cancer Therapeutics

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 June 2024) | Viewed by 15598

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Prof. Dr. Kang-Nan Wang

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State Key Laboratory of Crystal Materials, Shandong University, Jinan 250100, China
Interests: sensing and imaging; photodynamic diagnostic
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Dear Colleagues,

Increasing applications of functional targeting molecules in cells and organisms have been reported in recent years. These molecules are designed as sensing, imaging, anti-inflammation, and antineoplastic agents. Among them, some insightful researchers even integrate multiple functionalities in one molecule. Researchers continuously explore novel functional molecules for disease therapeutics, including targeted drug delivery systems, imaging agents for tumor/inflammation characterization, and molecular probes for detecting specific biomarkers associated with cancer and other diseases. By harnessing the unique properties of these functional molecules, such as their ability to emit fluorescence or generate a signal in response to specific conditions, researchers gain valuable insights into the intricate workings of cells and tissues as diagnosis probes. By selectively targeting cancer cells, these materials act as drugs that deliver a lethal dose of reactive oxygen species, leading to localized cell death and tumor destruction. In conclusion, the development of functional molecules for sensing, imaging, tracing, and cancer therapeutics has transformed the landscape of medical research and diagnostics. Manuscripts may cover a range of topics, including but not limited to the following:

Preparing and screening functional molecules of various applications.
Amplifying functional molecules with an affinity for the target substances, including but not limited to proteins and nucleic acid.
Drug delivery systems, including targeted molecules or targeted subcellular localization.
Potential cancer or inflammation-related biomarkers discovery and their pharmaceutical evaluation.

Prof. Dr. Kang-Nan Wang
Guest Editor

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Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

functional molecules
fluorescence imaging
targeted therapy of cancer
pharmaceutical evaluation

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Published Papers (11 papers)

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21 pages, 6402 KiB

Open AccessArticle

Targeting CD36-Mediated Lipid Metabolism by Selective Inhibitor-Augmented Antitumor Immune Responses in Oral Cancer

by Mayu Takaichi, Hidetake Tachinami, Danki Takatsuka, Amirmoezz Yonesi, Kotaro Sakurai, Muhammad Irfan Rasul, Shuichi Imaue, Shin-Ichi Yamada, Muhammad Ruslin, Manabu Yamazaki, Jun-Ichi Tanuma, Makoto Noguchi and Kei Tomihara

Int. J. Mol. Sci. 2024, 25(17), 9438; https://doi.org/10.3390/ijms25179438 - 30 Aug 2024

Viewed by 925

Abstract

The fatty acid receptor CD36 is expressed on various malignant cells and is suggested to contribute to tumor progression. CD36 is also expressed by several immune cells and involved in immune responses and may be a potential target in cancer immunotherapy. In this study, we investigated whether the selective inhibition of CD36 can inhibit tumor progression and facilitate an antitumor immune response in oral squamous carcinoma cells (OSCCs). We assessed the effects of sulfosuccinimidyl oleate sodium (SSO), a CD36 inhibitor, on the proliferation apoptosis and alteration in tumor cell surface expression levels of immune accessory molecules in vitro. We also assessed whether SSO-treated OSCCs could promote a T cell response via a Mixed Lymphocyte Reaction (MLR) assay. We also investigated the direct antitumor effects and immunomodulatory effects of SSO using a mouse oral cancer OSCC model. SSO treatment significantly inhibited OSCC proliferation, increased apoptotic cell death, and upregulated the cell surface expression of several immune accessory molecules, including CD83, MHC-Class II, and PD-L1. SSO-treated OSCCs augmented T cell proliferation following MLR. In vivo SSO administration significantly attenuated mouse tumor growth with an increased proportion of immune cells, including CD4⁺ T, CD8⁺ T, and dendritic cells; it also decreased the proportion of immune suppressive cells, such as myeloid-derived suppressor and regulatory T cells. These results suggest that the selective inhibition of CD36 can induce direct and indirect antitumor effects by facilitating host antitumor immune responses in OSCCs. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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12 pages, 988 KiB

Open AccessArticle

Transferrin-Conjugated Nanostructured Lipid Carriers for Targeting Artemisone to Melanoma Cells

by Njoud Altuwaijri and Eman Atef

Int. J. Mol. Sci. 2024, 25(16), 9119; https://doi.org/10.3390/ijms25169119 - 22 Aug 2024

Viewed by 819

Abstract

We report a successful formulation of Artemisone (ATM) in transferrin (Tf)-conjugated nanostructured lipid carriers (NLCs), achieving nearly a five-times increase in cell toxicity. The escalating cost of new drug discoveries led to the repurposing of approved drugs for new indications. This study incorporated Artemisone, an antimalarial drug, into a nanostructured lipid carrier (NLC) and tested for possible anticancer effects. The aim was to develop NLCs, and transferrin-conjugated NLCs (NLC-Tf) encapsulating Artemisone to enhance its delivery and anticancer activity. NLC formulations were prepared using high-pressure homogenization followed by ultrasonication and were characterized by particle size, zeta potential, and PDI. The conjugation of (Tf) to (NLC) was confirmed using IR, and the anticancer activity was tested using MTS assay. All formulations were in the nanometer size range (140–167 nm) with different zeta potential values. IR spectroscopy confirmed the successful conjugation of transferrin to NLC. Upon testing the formulations on melanoma cell lines using MTS assay, there was a significant decrease in viability and an increase in the encapsulated ATM-Tf toxicity compared to positive control ATM. The NLCs presented a promising potential carrier for delivering ATM to melanoma cells, and further conjugation with Tf significantly improved the ATM cytotoxicity. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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13 pages, 6840 KiB

Open AccessArticle

Development of Bivalent Aptamer-DNA Carrier-Doxorubicin Conjugates for Targeted Killing of Esophageal Squamous Cell Carcinoma Cells

by Tianlu Zhang, Kai Yin, Xidong Niu, Xue Bai, Zhaoting Wang, Mengmeng Ji and Baoyin Yuan

Int. J. Mol. Sci. 2024, 25(14), 7959; https://doi.org/10.3390/ijms25147959 - 21 Jul 2024

Viewed by 1071

Abstract

Esophageal cancer ranks the seventh in cancer incidence and the sixth in cancer death. Esophageal squamous cell carcinoma (ESCC) accounts for approximately 90% of the total cases of esophageal cancer. Chemotherapy is the most effective drug-based method for treatment of esophageal cancer. However, severe side effects of traditional chemotherapy limit its treatment efficacy. Targeted chemotherapy can deliver chemotherapeutic drugs to cancer cells and specifically kill these cells with reduced side effects. In the work, the bivalent aptamer-DNA carrier (BAD) was designed by using an ESCC cell-specific aptamer as the recognition molecule and a GC base-rich DNA sequence as the drug carrier. With doxorubicin (Dox) as chemotherapeutic drugs, the bivalent aptamer-DNA-Dox conjugate (BADD) was constructed for targeted killing of ESCC cells. Firstly, the truncated A2(35) aptamer with a retained binding ability was obtained through optimization of an intact A2(80) aptamer and was used to fuse with DNA carrier sequences for constructing the BAD through simple DNA hybridization. The results of gel electrophoresis and flow cytometry analysis showed that the BAD was successfully constructed and had a stronger binding affinity than monovalent A2(35). Then, the BAD was loaded with Dox drugs to construct the BADD through noncovalent intercalation. The results of fluorescence spectra and flow cytometry assays showed that the BADD was successfully constructed and can bind to target cells strongly. Confocal imaging further displayed that the BADD can be specifically internalized into target cells and release Dox. The results of CCK-8 assays, Calcein AM/PI staining, and wound healing assays demonstrated that the BADD can specifically kill target cells, but not control cells. Our results demonstrate that the developed BADD can specifically deliver doxorubicin to target ESCC cells and selectively kill these cells, offering a potentially effective strategy for targeted chemotherapy of ESCC. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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17 pages, 4780 KiB

Open AccessArticle

Synthesis, Characterization, Cytotoxicity, Cellular Imaging, Molecular Docking, and ADMET Studies of Piperazine-Linked 1,8-Naphthalimide-Arylsulfonyl Derivatives

by Ashanul Haque, Khalaf M. Alenezi, Ahmed Al-Otaibi, Abdulmohsen Khalaf Dhahi Alsukaibi, Ataur Rahman, Ming-Fa Hsieh, Mei-Wen Tseng and Wai-Yeung Wong

Int. J. Mol. Sci. 2024, 25(2), 1069; https://doi.org/10.3390/ijms25021069 - 15 Jan 2024

Cited by 3 | Viewed by 1720

Abstract

To reduce the mortality and morbidity associated with cancer, new cancer theranostics are in high demand and are an emerging area of research. To achieve this goal, we report the synthesis and characterization of piperazine-linked 1,8-naphthalimide-arylsulfonyl derivatives (SA1–SA7). These compounds were synthesized in good yields following a two-step protocol and characterized using multiple analytical techniques. In vitro cytotoxicity and fluorescent cellular imaging of the compounds were assessed against non-cancerous fibroblast (3T3) and breast cancer (4T1) cell lines. Although the former study indicated the safe nature of the compounds (viability = 82–95% at 1 μg/mL), imaging studies revealed that the designed probes had good membrane permeability and could disperse in the whole cell cytoplasm. In silico studies, including molecular docking, molecular dynamics (MD) simulation, and ADME/Tox results, indicated that the compounds had the ability to target CAIX-expressing cancers. These findings suggest that piperazine-linked 1,8-naphthalimide-arylsulfonyl derivatives are potential candidates for cancer theranostics and a valuable backbone for future research. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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17 pages, 3667 KiB

Open AccessArticle

POSS Engineering of Multifunctional Nanoplatforms for Chemo-Mild Photothermal Synergistic Therapy

by Zhengye Gu, Xiaochuan Geng, Shanyi Guang and Hongyao Xu

Int. J. Mol. Sci. 2024, 25(2), 1012; https://doi.org/10.3390/ijms25021012 - 13 Jan 2024

Cited by 1 | Viewed by 1252

Abstract

Chemo-mild photothermal synergistic therapy can effectively inhibit tumor growth under mild hyperthermia, minimizing damage to nearby healthy tissues and skin while ensuring therapeutic efficacy. In this paper, we develop a multifunctional study based on polyhedral oligomeric sesquisiloxane (POSS) that exhibits a synergistic therapeutic effect through mild photothermal and chemotherapy treatments (POSS-SQ-DOX). The nanoplatform utilizes SQ-N as a photothermal agent (PTA) for mild photothermal, while doxorubicin (DOX) serves as the chemotherapeutic drug for chemotherapy. By incorporating POSS into the nanoplatform, we successfully prevent the aggregation of SQ-N in aqueous solutions, thus maintaining its excellent photothermal properties both in vitro and in vivo. Furthermore, the introduction of polyethylene glycol (PEG) significantly enhances cell permeability, which contributes to the remarkable therapeutic effect of POSS-SQ-DOX NPs. Our studies on the photothermal properties of POSS-SQ-DOX NPs demonstrate their high photothermal conversion efficiency (62.3%) and stability, confirming their suitability for use in mild photothermal therapy. A combination index value (CI = 0.72) verified the presence of a synergistic effect between these two treatments, indicating that POSS-SQ-DOX NPs exhibited significantly higher cell mortality (74.7%) and tumor inhibition rate (72.7%) compared to single chemotherapy and mild photothermal therapy. This observation highlights the synergistic therapeutic potential of POSS-SQ-DOX NPs. Furthermore, in vitro and in vivo toxicity tests suggest that the absence of cytotoxicity and excellent biocompatibility of POSS-SQ-DOX NPs provide a guarantee for clinical applications. Therefore, utilizing near-infrared light-triggering POSS-SQ-DOX NPs can serve as chemo-mild photothermal PTA, while functionalized POSS-SQ-DOX NPs hold great promise as a novel nanoplatform that may drive significant advancements in the field of chemo-mild photothermal therapy. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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18 pages, 12448 KiB

Open AccessArticle

Design, Synthesis, and Antitumor Activity Evaluation of Proteolysis-Targeting Chimeras as Degraders of Extracellular Signal-Regulated Kinases 1/2

by Pengming Pan, Yichao He, Tongtong Geng, Zhongtang Li, Zhongjun Li and Xiangbao Meng

Int. J. Mol. Sci. 2023, 24(22), 16290; https://doi.org/10.3390/ijms242216290 - 14 Nov 2023

Cited by 2 | Viewed by 1587

Abstract

Inhibition of the extracellular signal-regulated kinases 1/2 (ERK1/2) alone or in combination with other targets has emerged as a promising treatment strategy for a variety of human tumors. In addition to the development of inhibitors, the development of ERK1/2 degraders is an alternative approach to decrease its activity. We synthesized proteolysis-targeting chimeras (PROTACs) as effective ERK1/2 degraders, among which B1-10J showed high degradative activity, with DC₅₀ of 102 nM and cytotoxic IC₅₀ of 2.2 μM against HCT116 cells. Moreover, B1-10J dose-dependently inhibited tumor cell migration. Xenograft experiments in nude mice demonstrated that B1-10J inhibited HCT116 tumor cell growth and achieved significant regression of tumors at a daily dose of 25 mg/kg. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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29 pages, 8444 KiB

Open AccessArticle

Activation of Chaperone-Mediated Autophagy Inhibits the Aryl Hydrocarbon Receptor Function by Degrading This Receptor in Human Lung Epithelial Carcinoma A549 Cells

by Rui Xiong, Dan Shao, Sandra Do and William K. Chan

Int. J. Mol. Sci. 2023, 24(20), 15116; https://doi.org/10.3390/ijms242015116 - 12 Oct 2023

Viewed by 1662

Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor and a substrate protein of a Cullin 4B E3 ligase complex responsible for diverse cellular processes. In the lung, this receptor is responsible for the bioactivation of benzo[a]pyrene during tumorigenesis. Realizing that the AHR function is affected by its expression level, we are interested in the degradation mechanism of AHR in the lung. Here, we have investigated the mechanism responsible for AHR degradation using human lung epithelial A549 cells. We have observed that the AHR protein levels increase in the presence of chloroquine (CQ), an autophagy inhibitor, in a dose-dependent manner. Treatment with 6-aminonicotinamide (6-AN), a chaperone-mediated autophagy (CMA) activator, decreases AHR protein levels in a concentration-dependent and time-dependent manner. This decrease suppresses the ligand-dependent activation of the AHR target gene transcription, and can be reversed by CQ but not MG132. Knockdown of lysosome-associated membrane protein 2 (LAMP2), but not autophagy-related 5 (ATG5), suppresses the chloroquine-mediated increase in the AHR protein. AHR is resistant to CMA when its CMA motif is mutated. Suppression of the epithelial-to-mesenchymal transition in A549 cells is observed when the AHR gene is knocked out or the AHR protein level is reduced by 6-AN. Collectively, we have provided evidence supporting that AHR is continuously undergoing CMA and activation of CMA suppresses the AHR function in A549 cells. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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20 pages, 10553 KiB

Open AccessArticle

Activation of G-Protein-Coupled Estrogen Receptor 1 (GPER1) Reduces Progression of Vulvar Carcinoma Cells

by Johanna Loris, Lena Hanesch, Gerd Bauerschmitz, Julia Gallwas and Carsten Gründker

Int. J. Mol. Sci. 2023, 24(18), 13705; https://doi.org/10.3390/ijms241813705 - 5 Sep 2023

Cited by 1 | Viewed by 1258

Abstract

Whether G protein-coupled estrogen receptor 1 (GPER1) is tumor-promoting or tumor-suppressive depends in part on tumor entity. Little is known about the function of GPER1 in vulvar carcinoma. In this work, we aim to clarify what role GPER1 plays in vulvar cancer, tumor-promoting or tumor-suppressive. Localization of GPER1 in A431 and CAL-39 vulvar carcinoma cells was examined by immunofluorescence. Using a tissue microarray of vulvar neoplasias, the correlation between GPER1 expression and grade of malignancy was investigated. A431 and CAL-39 cells were treated either with GPER1 agonist G1 or antagonist G36. Proliferation was quantified by BrdU assay and viability examined using Resazurin assay. Morphological changes were analyzed by microscopy and measured using ImageJ. Cell migration was analyzed by gap closure assay. Clonogenic potential was tested by colony and sphere formation. Expression of estrogen receptors was examined by Western blot. GPER1 was found consistently expressed in vulvar neoplasia tissues. The immune-reactive score was found to be significantly higher in tissue samples of lymph node metastases and neoplasias with grade 3. In A431 and CAL-39 vulvar carcinoma cells, GPER1 expression was mainly found in the cytoplasm and nuclei. Treatment of A431 and CAL-39 cells with GPER1 agonist G1 resulted in a decrease in proliferation and migration. In addition, colony formation and tumor sphere formation were reduced. Furthermore, morphological signs of necrosis and reduction in cell viability after G1 treatment were observed. The GPER1 antagonist G36 did not have significant effects on vulvar carcinoma cells. Neither agonist G1 nor antagonist G36 treatment resulted in altered expression of estrogen receptors. Activation of GPER1 with GPER1 agonist G1 reduces the tumorigenic potential of the vulvar carcinoma cells. It can be deduced from this that GPER1 appears to have a tumor-suppressive effect in vulvar carcinoma. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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Review

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19 pages, 906 KiB

Open AccessReview

Enhancing Colorectal Cancer Immunotherapy: The Pivotal Role of Ferroptosis in Modulating the Tumor Microenvironment

by Yanqing Li and Xiaofei Cheng

Int. J. Mol. Sci. 2024, 25(17), 9141; https://doi.org/10.3390/ijms25179141 - 23 Aug 2024

Viewed by 1374

Abstract

Colorectal cancer (CRC) represents a significant challenge in oncology, with increasing incidence and mortality rates worldwide, particularly among younger adults. Despite advancements in treatment modalities, the urgent need for more effective therapies persists. Immunotherapy has emerged as a beacon of hope, offering the potential for improved outcomes and quality of life. This review delves into the critical interplay between ferroptosis, an iron-dependent form of regulated cell death, and immunotherapy within the CRC context. Ferroptosis’s influence extends beyond tumor cell fate, reshaping the tumor microenvironment (TME) to enhance immunotherapy’s efficacy. Investigations into Ferroptosis-related Genes (OFRGs) reveal their pivotal role in modulating immune cell infiltration and TME composition, closely correlating with tumor responsiveness to immunotherapy. The integration of ferroptosis inducers with immunotherapeutic strategies, particularly through novel approaches like ferrotherapy and targeted co-delivery systems, showcases promising avenues for augmenting treatment efficacy. Furthermore, the expression patterns of OFRGs offer novel prognostic tools, potentially guiding personalized and precision therapy in CRC. This review underscores the emerging paradigm of leveraging ferroptosis to bolster immunotherapy’s impact, highlighting the need for further research to translate these insights into clinical advancements. Through a deeper understanding of the ferroptosis-immunotherapy nexus, new therapeutic strategies can be developed, promising enhanced efficacy and broader applicability in CRC treatment, ultimately improving patient outcomes and quality of life in the face of this formidable disease. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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18 pages, 1509 KiB

Open AccessReview

Assessment of the Impact of Trace Essential Metals on Cancer Development

by Aleksandra Górska, Agnieszka Markiewicz-Gospodarek, Mateusz Trubalski, Marta Żerebiec, Julia Poleszak and Renata Markiewicz

Int. J. Mol. Sci. 2024, 25(13), 6842; https://doi.org/10.3390/ijms25136842 - 21 Jun 2024

Viewed by 1017

Abstract

This study examines the impact of zinc, copper, cobalt, iron, and manganese on cancer development, considering their dual roles as potential promoters or inhibitors within tumorigenesis. A comprehensive analysis of existing literature and experimental data is conducted to elucidate the intricate relationship between these trace elements and cancer progression. The findings highlight the multifaceted effects of zinc, copper, cobalt, iron, and manganese on various aspects of cancer development, including cell proliferation, angiogenesis, and metastasis. Understanding the nuanced interactions between these trace elements and cancer could offer crucial insights into tumorigenesis mechanisms and facilitate the identification of novel biomarkers and therapeutic targets for cancer prevention and treatment strategies. This research underscores the importance of considering the roles of essential trace elements in cancer biology and may ultimately contribute to advancements in precision medicine approaches for combating cancer. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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29 pages, 2026 KiB

Open AccessReview

Exploring the Key Signaling Pathways and ncRNAs in Colorectal Cancer

by Yun Ju Lee, Woo Ryung Kim, Eun Gyung Park, Du Hyeong Lee, Jung-min Kim, Hae Jin Shin, Hyeon-su Jeong, Hyun-Young Roh and Heui-Soo Kim

Int. J. Mol. Sci. 2024, 25(8), 4548; https://doi.org/10.3390/ijms25084548 - 21 Apr 2024

Cited by 5 | Viewed by 2181

Abstract

Colorectal cancer (CRC) is the third most prevalent cancer to be diagnosed, and it has a substantial mortality rate. Despite numerous studies being conducted on CRC, it remains a significant health concern. The disease-free survival rates notably decrease as CRC progresses, emphasizing the urgency for effective diagnostic and therapeutic approaches. CRC development is caused by environmental factors, which mostly lead to the disruption of signaling pathways. Among these pathways, the Wingless/Integrated (Wnt) signaling pathway, Phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) signaling pathway, Mitogen-Activated Protein Kinase (MAPK) signaling pathway, Transforming Growth Factor-β (TGF-β) signaling pathway, and p53 signaling pathway are considered to be important. These signaling pathways are also regulated by non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs). They have emerged as crucial regulators of gene expression in CRC by changing their expression levels. The altered expression patterns of these ncRNAs have been implicated in CRC progression and development, suggesting their potential as diagnostic and therapeutic targets. This review provides an overview of the five key signaling pathways and regulation of ncRNAs involved in CRC pathogenesis that are studied to identify promising avenues for diagnosis and treatment strategies. Full article

(This article belongs to the Special Issue Functional Molecules in Tracing and Cancer Therapeutics)

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