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Adjuvant Therapies for Cancer Treatment

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A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 24 February 2025 | Viewed by 19091

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Special Issue Editors

Prof. Dr. Fuyi Wang

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Guest Editor

CAS Key Laboratory of Analytical Chemistry for Living Biosystems, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190, China
Interests: anticancer drug design; nutural bioactive products; interactomics of drugs; chemical biology of drugs; mass spectrometry; mass spectrometry imaging; chemical proteomics

Dr. Andréia Machado Leopoldino

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Guest Editor

Department of Clinical Analyses, Toxicology and Food Sciences, School of Pharmaceutical Sciences of Ribeirão Preto, Universidade de São Paulo (USP), Sao Paulo 14040-903, Brazil
Interests: new therapies; targeting signaling pathways; biomarkers; drug resistance; cancer stem cell; adjuvant therapy

Special Issue Information

Dear Colleagues,

To improve cancer survival and prevent the recurrence of the disease and metastasis, we still need to find new compounds and therapeutic strategies, as well as apply drug repurposing and combined therapies. This means finding better adjuvant therapy to improve cancer cures in the next decade.

Adjuvant therapy may take the form of chemotherapy, radiotherapy, biological therapy, hormone therapy, and targeted therapy.

Adjuvant therapy is used after an initial treatment (such as surgery) or before as a neoadjuvant. Both applications have advantages (such as reducing the tumor size, preventing tumor cells to spread/metastasis, and eliminating any remaining malignant cells after surgery and disease recurrence) and disadvantages (such as serious side effects).

Omics studies and biological approaches have brought a lot of knowledge about alterations and signaling deregulations in several cancer types and profiles related to outcome and drug efficacy. Cancer resistance occurs in different types of tumors and patients under different treatments where some therapies are associated with specific resistance mechanisms (such as drug efflux, autophagy, apoptosis blockage, metabolism reprogramming, mutations, and stemness). However, the next steps in oncology will be to connect molecular data with clinical practice and offer a potential and specific protocol to the patient for cancer treatment.

This Special Issue is dedicated to illustrating the new findings in adjuvant therapy applied for cancer treatment and highlights the gaps and new directions in this field.

Prof. Dr. Fuyi Wang
Dr. Andréia Machado Leopoldino
Guest Editors

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Keywords

drug repurposing
combined therapies
new compounds
drug resistance
chemosensitization
antitumoral strategies

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Published Papers (9 papers)

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Research

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14 pages, 4738 KiB

Open AccessArticle

The Role of ADCY1 in Regulating the Sensitivity of Platinum-Based Chemotherapy in NSCLC

by Ting Zou, Jun-Yan Liu, Zhao-Qian Liu, Di Xiao and Juan Chen

Pharmaceuticals 2024, 17(9), 1118; https://doi.org/10.3390/ph17091118 - 24 Aug 2024

Cited by 1 | Viewed by 984

Abstract

Lung cancer has the highest fatality rate among malignant tumors in the world. Finding new biomarkers of drug resistance is of great importance in the prognosis of lung cancer patients. We found that the polymorphisms of Adenylate Cyclase 1 (ADCY1) are significantly associated with platinum-based chemotherapy resistance in lung cancer patients in our previous research. In this study, we wanted to identify the mechanism of ADCY1 affecting platinum resistance. We used an MTT assay to find if the expression of ADCY1 is associated with the sensitivity of cisplatin in A549, H1299, and A549-DDP cells. Then, we performed CCK-8 tests to detect the absorbance of these cells stimulated by ADCY1, which can discover the cell proliferation that is affected by ADCY1. We investigated cell apoptosis and cell cycles regulated by ADCY1 through the flow cytometry assay. RNA sequencing was used to find the downstream genes affected by ADCY1 which may be associated with drug resistance in lung cancer patients. ADCY1 has higher expression in lung cancer cells than in normal cells. ADCY1 can affect cisplatin resistance in lung cancer cells by regulating cell proliferation, cell apoptosis, and the cell cycle. It may control cell apoptosis by regulating the classical apoptosis biomarkers Bax and Bcl2. Our study showed that ADCY1 may be a new biomarker in the prognosis of lung cancer patients. Much work remains to be carried out to clarify the mechanism in this important emerging field. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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12 pages, 3003 KiB

Open AccessArticle

Enhanced Antitumor Activity by the Combination of Dasatinib and Selinexor in Chronic Myeloid Leukemia

by Mariarita Spampinato, Tatiana Zuppelli, Ilaria Dulcamare, Lucia Longhitano, Domenico Sambataro, Annalisa Santisi, Amer M. Alanazi, Ignazio A. Barbagallo, Nunzio Vicario, Rosalba Parenti, Alessandra Romano, Giuseppe Musumeci, Giovanni Li Volti, Giuseppe A. Palumbo, Francesco Di Raimondo, Anna Nicolosi, Sebastiano Giallongo and Vittorio Del Fabro

Pharmaceuticals 2024, 17(7), 894; https://doi.org/10.3390/ph17070894 - 5 Jul 2024

Cited by 1 | Viewed by 1061

Abstract

Background: Chronic myeloid leukemia is a hematological malignancy characterized by the abnormal proliferation of leukemic cells. Despite significant progress with tyrosine kinase inhibitors, such as Dasatinib, resistance remains a challenge. The aim of the present study was to investigate the potential of Selinexor, an Exportin-1 inhibitor, to improve TKI effectiveness on CML. Methods: Human CML cell lines (LAMA84 and K562) were treated with Selinexor, Dasatinib, or their combination. Apoptosis, mitochondrial membrane potential, and mitochondrial mass were assessed using flow cytometry. Real-time RT-PCR was used to evaluate the expression of genes related to mitochondrial function. Western blot and confocal microscopy examined PINK and heme oxygenase-1 (HO-1) protein levels. Results: Selinexor induced apoptosis and mitochondrial depolarization in CML cell lines, reducing cell viability. The Dasatinib/Selinexor combination further enhanced cytotoxicity, modified mitochondrial fitness, and downregulated HO-1 nuclear translocation, which has been associated with drug resistance in different models. Conclusions: In conclusion, this study suggests that Dasatinib/Selinexor could be a promising therapeutic strategy for CML, providing new insights for new targeted therapies. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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30 pages, 8533 KiB

Open AccessArticle

Evaluating the Role of Neddylation Modifications in Kidney Renal Clear Cell Carcinoma: An Integrated Approach Using Bioinformatics, MLN4924 Dosing Experiments, and RNA Sequencing

by Dequan Liu, Guangzhen Wu, Shijin Wang, Xu Zheng and Xiangyu Che

Pharmaceuticals 2024, 17(5), 635; https://doi.org/10.3390/ph17050635 - 15 May 2024

Cited by 1 | Viewed by 1484

Abstract

Background: Neddylation, a post-translational modification process, plays a crucial role in various human neoplasms. However, its connection with kidney renal clear cell carcinoma (KIRC) remains under-researched. Methods: We validated the Gene Set Cancer Analysis Lite (GSCALite) platform against The Cancer Genome Atlas (TCGA) database, analyzing 33 cancer types and their link with 17 neddylation-related genes. This included examining copy number variations (CNVs), single nucleotide variations (SNVs), mRNA expression, cellular pathway involvement, and methylation. Using Gene Set Variation Analysis (GSVA), we categorized these genes into three clusters and examined their impact on KIRC patient prognosis, drug responses, immune infiltration, and oncogenic pathways. Afterward, our objective is to identify genes that exhibit overexpression in KIRC and are associated with an adverse prognosis. After pinpointing the specific target gene, we used the specific inhibitor MLN4924 to inhibit the neddylation pathway to conduct RNA sequencing and related in vitro experiments to verify and study the specificity and potential mechanisms related to the target. This approach is geared towards enhancing our understanding of the prognostic importance of neddylation modification in KIRC. Results: We identified significant CNV, SNV, and methylation events in neddylation-related genes across various cancers, with notably higher expression levels observed in KIRC. Cluster analysis revealed a potential trade-off in the interactions among neddylation-related genes, where both high and low levels of gene expression are linked to adverse prognoses. This association is particularly pronounced concerning lymph node involvement, T stage classification, and Fustat score. Simultaneously, our research discovered that PSMB10 exhibits overexpression in KIRC when compared to normal tissues, negatively impacting patient prognosis. Through RNA sequencing and in vitro assays, we confirmed that the inhibition of neddylation modification could play a role in the regulation of various signaling pathways, thereby influencing the prognosis of KIRC. Moreover, our results underscore PSMB10 as a viable target for therapeutic intervention in KIRC, opening up novel pathways for the development of targeted treatment strategies. Conclusion: This study underscores the regulatory function and potential mechanism of neddylation modification on the phenotype of KIRC, identifying PSMB10 as a key regulatory target with a significant role in influencing the prognosis of KIRC. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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20 pages, 3874 KiB

Open AccessArticle

Potential Antitumor Activity of Combined Lycopene and Sorafenib against Solid Ehrlich Carcinoma via Targeting Autophagy and Apoptosis and Suppressing Proliferation

by Thanaa A. El-Masry, Maysa M. F. El-Nagar, Nageh A. El Mahdy, Fatemah A. Alherz, Reham Taher and Enass Y. Osman

Pharmaceuticals 2024, 17(4), 527; https://doi.org/10.3390/ph17040527 - 19 Apr 2024

Cited by 3 | Viewed by 1622

Abstract

An FDA-approved kinase inhibitor called sorafenib (SOR) is used to treat primary kidney and liver cancer as well as to stop the spread of advanced breast cancer. Side effects from SOR, such as palmar–plantar erythrodysesthesia syndrome, can negatively impact an individual’s quality of life. There are a lot of data supporting the importance of lycopene (LYC) in preventing cancer. The antitumor properties of the combination of sorafenib and lycopene were examined in this study. A viability test against MDA-MB-231 was used to assess the anticancer efficacy of sorafenib, lycopene, and their combination in vitro. Moreover, a cell cycle analysis and Annexin-V/PI double staining were performed by using flow cytometry. In addition, the protein level of JNK-1, ERK-1, Beclin-1, P38, and P53 of the MDA-MB-231 cell line was estimated using ELISA kits. In addition, mice with SEC were divided into four equal groups at random (n = 10) to investigate the possible processes underlying the in vivo antitumor effect. Group IV (SEC-SOR-LYC) received SOR (30 mg/kg/day, p.o.) and LYC (20 mg/kg/day, p.o.); Group I received the SEC control; Group II received SEC-SOR (30 mg/kg/day, p.o.); and Group III received SEC-LYC (20 mg/kg/day, p.o.). The findings demonstrated that the combination of sorafenib and lycopene was superior to sorafenib and lycopene alone in causing early cell cycle arrest, suppressing the viability of cancer cells, and increasing cell apoptosis and autophagy. Likewise, the combination of sorafenib and lycopene demonstrated inhibition of the levels of Bcl-2, Ki-67, VEGF, IL-1β, and TNF-α protein. Otherwise, the quantities of the proteins BAX, P53, and caspase 3 were amplified. Furthermore, the combined treatment led to a substantial increase in TNF-α, caspase 3, and VEGF gene expression compared to the equivalent dosages of monotherapy. The combination of sorafenib and lycopene enhanced apoptosis and reduced inflammation, as seen by the tumor’s decreased weight and volume, hence demonstrating its potential anticancer effect. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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11 pages, 473 KiB

Open AccessArticle

Relation of Statin Use with Esophageal Cancer

by Sarang Jang, Hyo Geun Choi, Mi Jung Kwon, Ji Hee Kim, Joo-Hee Kim and So Young Kim

Pharmaceuticals 2023, 16(6), 900; https://doi.org/10.3390/ph16060900 - 19 Jun 2023

Viewed by 1593

Abstract

The present study evaluated the association of long-term statin use with the diagnosis and mortality of esophageal cancer in a Korean population. The Korean National Health Insurance Service-Health Screening Cohort from 2002 to 2019 was enrolled. Esophageal cancer patients were matched with control participants for demographic variables. The statin prescription histories were collected and grouped into <180 days, 180 to 545 days, and >545 days of duration. Propensity score overlap weighting was applied to minimize the bias between the esophageal cancer and control groups. The odds ratios (ORs) of the duration of statin use for esophageal cancer were analyzed using propensity score overlap weighted multivariable logistic regression analysis. The esophageal cancer group was classified as dead and surviving patients, and the ORs of the duration of statin use for the mortality of esophageal cancer were analyzed in an identical manner. Secondary analyses were conducted according to comorbid factors. Patients with esophageal cancer did not show lower odds for the duration of statin prescription in the overall study population (OR = 1.30, 95% CI = 1.03–1.65, p = 0.027 for 180 to 545 days and OR = 1.29, 95% CI = 1.08–1.55, p = 0.006 for >545 days). Subgroups of nonsmokers, past and current smokers, alcohol consumption ≥ 1 time a week, SBP < 140 mmHg and DBP < 90 mmHg, fasting blood glucose ≥ 100 mg/dL, total cholesterol ≥ 200 mg/dL, CCI score = 0, and nondyslipidemia history demonstrated low odds for the duration of statin prescription. Both types of statins, hydrophilic and lipophilic statins, were not related to a lower rate of esophageal cancer. The mortality of esophageal cancer was not associated with the duration of statin prescription. A subgroup with total cholesterol ≥ 200 mg/dL showed lower odds of statin prescription for mortality of esophageal cancer. The duration of statin prescription was not related to a lower rate or mortality of esophageal cancer in the adult Korean population. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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Review

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30 pages, 1852 KiB

Open AccessReview

The Pivotal Role of Preclinical Animal Models in Anti-Cancer Drug Discovery and Personalized Cancer Therapy Strategies

by Haochuan Guo, Xinru Xu, Jiaxi Zhang, Yajing Du, Xinbing Yang, Zhiheng He, Linjie Zhao, Tingming Liang and Li Guo

Pharmaceuticals 2024, 17(8), 1048; https://doi.org/10.3390/ph17081048 - 9 Aug 2024

Viewed by 3289

Abstract

The establishment and utilization of preclinical animal models constitute a pivotal aspect across all facets of cancer research, indispensably contributing to the comprehension of disease initiation and progression mechanisms, as well as facilitating the development of innovative anti-cancer therapeutic approaches. These models have emerged as crucial bridges between basic and clinical research, offering multifaceted support to clinical investigations. This study initially focuses on the importance and benefits of establishing preclinical animal models, discussing the different types of preclinical animal models and recent advancements in cancer research. It then delves into cancer treatment, studying the characteristics of different stages of tumor development and the development of anti-cancer drugs. By integrating tumor hallmarks and preclinical research, we elaborate on the path of anti-cancer drug development and provide guidance on personalized cancer therapy strategies, including synthetic lethality approaches and novel drugs widely adopted in the field. Ultimately, we summarize a strategic framework for selecting preclinical safety experiments, tailored to experimental modalities and preclinical animal species, and present an outlook on the prospects and challenges associated with preclinical animal models. These models undoubtedly offer new avenues for cancer research, encompassing drug development and personalized anti-cancer protocols. Nevertheless, the road ahead continues to be lengthy and fraught with obstacles. Hence, we encourage researchers to persist in harnessing advanced technologies to refine preclinical animal models, thereby empowering these emerging paradigms to positively impact cancer patient outcomes. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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66 pages, 6931 KiB

Open AccessReview

Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts

by Tomas Koltai and Larry Fliegel

Pharmaceuticals 2024, 17(6), 744; https://doi.org/10.3390/ph17060744 - 6 Jun 2024

Cited by 1 | Viewed by 2858

Abstract

Rarely has a chemical elicited as much controversy as dichloroacetate (DCA). DCA was initially considered a dangerous toxic industrial waste product, then a potential treatment for lactic acidosis. However, the main controversies started in 2008 when DCA was found to have anti-cancer effects on experimental animals. These publications showed contradictory results in vivo and in vitro such that a thorough consideration of this compound’s in cancer is merited. Despite 50 years of experimentation, DCA’s future in therapeutics is uncertain. Without adequate clinical trials and health authorities’ approval, DCA has been introduced in off-label cancer treatments in alternative medicine clinics in Canada, Germany, and other European countries. The lack of well-planned clinical trials and its use by people without medical training has discouraged consideration by the scientific community. There are few thorough clinical studies of DCA, and many publications are individual case reports. Case reports of DCA’s benefits against cancer have been increasing recently. Furthermore, it has been shown that DCA synergizes with conventional treatments and other repurposable drugs. Beyond the classic DCA target, pyruvate dehydrogenase kinase, new target molecules have also been recently discovered. These findings have renewed interest in DCA. This paper explores whether existing evidence justifies further research on DCA for cancer treatment and it explores the role DCA may play in it. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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21 pages, 1504 KiB

Open AccessReview

Advances in IL-7 Research on Tumour Therapy

by Chunxue Fu, Xinqiang Zhang, Xinyu Zhang, Dan Wang, Shuxin Han and Zhenghai Ma

Pharmaceuticals 2024, 17(4), 415; https://doi.org/10.3390/ph17040415 - 25 Mar 2024

Cited by 1 | Viewed by 2292

Abstract

Interleukin-7 (IL-7) is a versatile cytokine that plays a crucial role in regulating the immune system’s homeostasis. It is involved in the development, proliferation, and differentiation of B and T cells, as well as being essential for the differentiation and survival of naïve T cells and the production and maintenance of memory T cells. Given its potent biological functions, IL-7 is considered to have the potential to be widely used in the field of anti-tumour immunotherapy. Notably, IL-7 can improve the tumour microenvironment by promoting the development of Th17 cells, which can in turn promote the recruitment of effector T cells and NK cells. In addition, IL-7 can also down-regulate the expression of tumour growth factor-β and inhibit immunosuppression to promote anti-tumour efficacy, suggesting potential clinical applications for anti-tumour immunotherapy. This review aims to discuss the origin of IL-7 and its receptor IL-7R, its anti-tumour mechanism, and the recent advances in the application of IL-7 in tumour therapy. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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24 pages, 2579 KiB

Open AccessReview

Exploring the mTOR Signalling Pathway and Its Inhibitory Scope in Cancer

by Suhail Ahmad Mir, Ashraf Dar, Saad Ali Alshehri, Shadma Wahab, Laraibah Hamid, Mohammad Ali Abdullah Almoyad, Tabasum Ali and Ghulam Nabi Bader

Pharmaceuticals 2023, 16(7), 1004; https://doi.org/10.3390/ph16071004 - 14 Jul 2023

Cited by 8 | Viewed by 3023

Abstract

Mechanistic target of rapamycin (mTOR) is a protein kinase that regulates cellular growth, development, survival, and metabolism through integration of diverse extracellular and intracellular stimuli. Additionally, mTOR is involved in interplay of signalling pathways that regulate apoptosis and autophagy. In cells, mTOR is assembled into two complexes, mTORC1 and mTORC2. While mTORC1 is regulated by energy consumption, protein intake, mechanical stimuli, and growth factors, mTORC2 is regulated by insulin-like growth factor-1 receptor (IGF-1R), and epidermal growth factor receptor (EGFR). mTOR signalling pathways are considered the hallmark in cancer due to their dysregulation in approximately 70% of cancers. Through downstream regulators, ribosomal protein S6 kinase β-1 (S6K1) and eukaryotic translation initiation factor 4E binding protein 1 (4E-BP1), mTORC1 influences various anabolic and catabolic processes in the cell. In recent years, several mTOR inhibitors have been developed with the aim of treating different cancers. In this review, we will explore the current developments in the mTOR signalling pathway and its importance for being targeted by various inhibitors in anti-cancer therapeutics. Full article

(This article belongs to the Special Issue Adjuvant Therapies for Cancer Treatment)

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