Immunotherapy and targeted therapy for cervical cancer: an update

Menderes, Gulden; Black, Jonathan; Schwab, Carlton L.; Santin, Alessandro D.

doi:10.1586/14737140.2016.1121108

Cited by 108 publications

(76 citation statements)

References 119 publications

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“…Targeted therapies based on the knowledge of the molecular pathogenesis of the disease and immunotherapy targeting human papillomavirus (HPV) oncoproteins, such as E6 and E7, showed some promising. 2,3 However, advanced-inoperable cervical cancer is still challenging due to increased percentage of regional and distant recurrences with dismal prognosis. Thus, better understanding of pathological changes and development of new treatment paradigm are strongly desirable.…”

Section: Introductionmentioning

confidence: 99%

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

Tang¹,

Liu²,

Zhang³

et al. 2020

DDDT

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Background: Shikonin, the main ingredient of Lithospermum erythrorhizon, has been reported to have antitumor effects via multiple targets and signaling pathways. However, the detailed mechanism underlying the effects in cervical cancer still remained unknown. Methods: MTT, wound-healing, transwell assays and flow cytometry experiments were used to measure cell growth, migration, invasion, and cell cycle analysis. Western blot was used to examine protein levels of Snail, Vimentin and E-cadherin. The expression level of miR-183-5p was measured via qRT-PCR. The E-cadherin promoter activity was detected via Secrete-PairTM Dual Luminescence Assay Kit. The transient transfection experiments were used for silencing of E-cadherin and overexpression of Snail genes. Tumor xenograft and bioluminescent imaging experiments were carried out to confirm the in vitro findings. Results: We showed that shikonin inhibited cell viability, migration and invasion, and induced cell cycle arrest in a dose-dependent manner in cervical cancer Hela and C33a cells. Mechanistically, we found that shikonin increased miR-183-5p expression and inhibited expression of transcription factor Snail protein. The mimics of miR-183-5p reduced, while the inhibitors of miR-183-5p reversed shikonin-inhibited Snail protein expression. In addition, shikonin decreased Vimentin, increased E-cadherin protein expressions and E-cadherin promoter activity, the latter was reversed in cells transfected with exogenous Snail overexpression vectors. Moreover, silencing of E-cadherin significantly abolished shikonin-inhibited cervical cancer cell growth. Similar findings were also observed in vivo using one xenograft mouse model. Conclusion: Our results show that shikonin inhibits EMT through inhibition of Snail and stimulation of miR-183-5p expressions, which resulted in induction of E-cadherin expression. Thus, blockade of EMT could be a novel mechanism underlying the anti-cervical cancer effects of shikonin.

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Section: Introductionmentioning

confidence: 99%

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

Tang¹,

Liu²,

Zhang³

et al. 2020

DDDT

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“…Immunotherapy will probably play a very important role in the future treatment of recurrent/metastatic CC. This tumor has several factors that could predict benefit from immunotherapy, such as the presence of antigens associated with the tumor (oncoproteins E6 and E7), high mutational load, or the presence of a lymphocytic infiltrate, mainly CD4 and CD8 [25].…”

Section: Futurementioning

confidence: 99%

SEOM clinical guidelines for cervical cancer (2019)

et al. 2020

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Cervical cancer (CC) is the fourth most common cancer in women worldwide, strongly linked to high-risk human papilloma virus infection. In high-income countries, the screening programs have dramatically decreased the incidence of CC; however, the lack of accessibility to them in developing countries makes CC an important cause of mortality. Clinical stage is the most relevant prognostic factor in CC. The new FIGO staging system published in 2018 is more accurate than the previous one since it takes into account the lymph node status. In early stages, the primary treatment is surgery-with some concerns recently raised regarding minimally invasive surgery because it might decrease survival-or radiotherapy, whereas concomitant chemo-radiotherapy is the conventional approach in locally advanced stages. For recurrent or metastatic CC, the combination of chemotherapy plus bevacizumab is the preferred therapy. Immunotherapy approach based on checkpoint inhibitors is evolving as the election therapy following failure to platinum therapy.

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“…2 Several types of HPV have identified in aggressive cervical cancer, whereas others are associated with dysplasia or carcinoma in situ. The known 13 types of high-risk HPV (HR-HPV) are 16,18,31,33,35,39,45,51,52,56,58,59 and 68. 2,3 Until now, the assessment of prognosis cervical cancer seen from a tumor marker.…”

Section: Cervical Cancermentioning

confidence: 99%

“…The fundamental approach based on specific recognition of tumor-associated antigen by cytotoxic T lymphocytes (CTL) which activated by presented dendritic cells. 57,58 About 30% of cervical cancer patients will experience failure therapy including surgery, radiotherapy and chemotherapy, as described above, survivin have an important role in that condition. 59 For that, targeting survivin immunological is very promising for treating cervical cancer and another cancer because of survivin suggested being a universal antigen for tumor based on the first evidence that survivin can induce specific CTL in vitro when the protein processed and presented by dendritic cells.…”

Section: Immunotherapy and Vaccinementioning

confidence: 99%

Survivin Clinical Features in Cervical Cancer

Rahman¹,

Wijaya²,

Novalentina³

2017

Mol Cell Biomed Sci

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Cervical cancer is the primary lethal malignancy for women worldwide, but because it develops over time, it would be one of the most preventable types of cancer. Dysregulation of apoptosis in cells plays a critical role in the malignancy development. Survivin is the smallest inhibitor apoptotic protein (IAP) which has an important part in regulating cell division and inhibitor of apoptosis. This review focused on survivin features in cervical cancer from mechanisms of malignancy relationship to human papillomavirus (HPV) infection through E6 oncogenic protein, role as a biomarker in diagnosis, prognosis, staging and prediction of metastasis, and also as a target for therapy. Regulation of survivin divided into two main groups; cell cycle dependent and cell cycle independent pathway to maintain life and death balance. Survivin expression is upregulated by E6 protein simultaneously repressing p53. Thus cancerous cervical tissue developed. Survivin is also upregulated in hypoxia, a common condition in many tumors and increased angiogenesis. Survivin plays a significant role in chemotherapy and radiation resistance in many cases of cervical cancer. As a target of therapy, survivin has a promising performance, suggested very specific, no issue of resistance and also enhance the effectiveness of chemo and radiation therapy. The goal of treatment is to lower survivin expression through transcription inhibition, immunotherapy based on cytotoxic T lymphocytes (CTL) activity and gene therapy.

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Immunotherapy and targeted therapy for cervical cancer: an update

Cited by 108 publications

References 119 publications

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

<p>Regulations of miR-183-5p and Snail-Mediated Shikonin-Reduced Epithelial-Mesenchymal Transition in Cervical Cancer Cells</p>

SEOM clinical guidelines for cervical cancer (2019)

Survivin Clinical Features in Cervical Cancer

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