Thymidine decreases the DNA damage and apoptosis caused by tumor‐treating fields in cancer cell lines

Jeong, Hyesun; Jo, Yunhui; Yoon, Myonggeun; Hong, Sunghoi

doi:10.1007/s13258-021-01105-z

Cited by 4 publications

(11 citation statements)

References 20 publications

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“…Thymidine is a vital drug when studying the S phase of DNA synthesis. Thymidine block, which achieves e cient synchronization of cell cultures in the S phase and does not alter cell growth or survival, is widely used to study the S phase of the cell cycle [25,[37][38][39][40] . However, the concentration of drug response varied among different types of cells.…”

Section: Discussionmentioning

confidence: 99%

Tubulin beta 4B chain is involved in the cell cycle process of mouse spermatogonia through CDK2

Mao

Zeng

Kuang

et al. 2022

Preprint

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Tubb4b (tubulin beta-4b chain) is essential for spermatogonia cell growth and development as a microtubule network protein, and its regulatory mechanism remains to be studied. To deeply understand the role of Tubb4b in spermatogonia cell proliferation and the cell cycle, we studied the role of spermatogonia in the control and TUBB4B-KO groups in different cell cycle phases by flow cytometry. We detected the crucial protein CDK2 in each stage by qRT–PCR and Western blotting. The results showed that under the induction of serum starvation, thymidine, and nocodazole under different conditions, mouse spermatogonia remained in the G0-G1 phase, S phase, and G2-M phase, respectively, and the change in the spermatogonia cycle in the Tubb4b-KO group was slower than that in the control group. In the study of cycle synchronization, it was found that the mRNA level of Cdk2 in the G2-M phase increased significantly (P < 0.001), accompanied by the accumulation of CDK2 protein. In the Tubb4b-KO group, the mRNA level of Cdk2 increased significantly in the G0-G1 phase (P < 0.05), decreased significantly in the S phase (P < 0.05) and was accompanied by the fluctuation of CDK2 protein. These data suggest that Tubb4b has the potential to play an important role during the spermatogonial cell cycle by affecting the fluctuating expression of CDK2.

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Section: Discussionmentioning

confidence: 99%

Tubulin beta 4B chain is involved in the cell cycle process of mouse spermatogonia through CDK2

Mao

Zeng

Kuang

et al. 2022

Preprint

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“…Similarly, TTFields significantly suppresses tumor proliferation and induces apoptosis when applied to the skin or abdomen [ 50 , 60 ] while the normal cells are unaffected [ 38 , 50 , 60 , 61 ]. However, normal cells HaCaT proliferated slightly after TTFields [ 62 ].…”

Section: Introductionmentioning

confidence: 99%

“…DNA damage repair and cell cycle arrest. TTFields inhibits tumor cells and causes DNA damage [ 62 ] but does not cause DNA double-strand breaks and cell cycle arrest in normal cells [ 57 , 61 ]. However, studies show that TTFields leads to G2/M arrest in IEC6 normal cells and tumor cells, but the increased degree varies with the duration of TTFields (0–24 hours/day) [ 57 ].…”

Section: Introductionmentioning

confidence: 99%

“…However, TTFields combined with the drugs does not necessarily and synergistically increase apoptosis. Thymidine attenuates TTFields-induced apoptosis in glioma cells [ 62 ]. TTFields restraints Osimertinib-induced apoptosis in lung adenocarcinoma cells and reduces the efficacy of Osimertinib [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

“…The application of TTFields in the G1 phase does not affect the portion of G1 phase; similarly, the same as in the M phase [ 66 ]. For the G1/S phase-blockade cell, TTFields could not induce cell death, apoptosis, and DNA damage [ 62 ], indicating that entering into the G1/S phase is necessary for TTFields to inhibit tumors.…”

Section: Introductionmentioning

confidence: 99%

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The schemes, mechanisms and molecular pathway changes of Tumor Treating Fields (TTFields) alone or in combination with radiotherapy and chemotherapy

et al. 2022

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Tumor Treating Fields (TTFields) is a physical therapy that uses moderate frequency (100–300 kHz) and low-intensity (1–3 V/cm) alternating electric fields to inhibit tumors. Currently, the Food and Drug Administration approves TTFields for treating recurrent or newly diagnosed glioblastoma (GBM) and malignant pleural mesothelioma (MPM). The classical mechanism of TTFields is mitotic inhibition by hindering the formation of tubulin and spindle. In addition, TTFields inhibits cell proliferation, invasion, migration and induces cell death, such as apoptosis, autophagy, pyroptosis, and cell cycle arrest. Meanwhile, it regulates immune function and changes the permeability of the nuclear membrane, cell membrane, and blood-brain barrier. Based on the current researches on TTFields in various tumors, this review comprehensively summarizes the in-vitro effects, changes in pathways and molecules corresponding to relevant parameters of TTFields (frequency, intensity, and duration). In addition, radiotherapy and chemotherapy are common tumor treatments. Thus, we also pay attention to the sequence and dose when TTFields combined with radiotherapy or chemotherapy. TTFields has inhibitory effects in a variety of tumors. The study of TTFields mechanism is conducive to subsequent research. How to combine common tumor therapy such as radiotherapy and chemotherapy to obtain the maximum benefit is also a problem that’s worthy of our attention.

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Anti-cancer mechanisms of action of therapeutic alternating electric fields (tumor treating fields [TTFields])

Shams

2022

Journal of Molecular Cell Biology

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Despite improved survival outcomes across many cancer types, the prognosis remains grim for certain solid organ cancers including glioblastoma and pancreatic cancer. Invariably in these cancers, the control achieved by time-limited interventions such as traditional surgical resection, radiation therapy, and chemotherapy is short-lived. A new form of anti-cancer therapy called therapeutic alternating electric fields (AEFs) or tumor treating fields (TTFields) has been shown, either by itself or in combination with chemotherapy, to have anti-cancer effects that translate to improved survival outcomes in patients. Although the pre-clinical and clinical data are promising, the mechanisms of TTFields are not fully elucidated. Many investigations are underway to better understand how and why TTFields is able to selectively kill cancer cells and impede their proliferation. The purpose of this review is to summarize and discuss the reported mechanisms of action of TTFields from pre-clinical studies (both in vitro and in vivo). An improved understanding of how TTFields works will guide strategies focused on the timing and combination of TTFields with other therapies, to further improve survival outcomes in patients with solid organ cancers.

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Thymidine decreases the DNA damage and apoptosis caused by tumor‐treating fields in cancer cell lines

Cited by 4 publications

References 20 publications

Tubulin beta 4B chain is involved in the cell cycle process of mouse spermatogonia through CDK2

Tubulin beta 4B chain is involved in the cell cycle process of mouse spermatogonia through CDK2

The schemes, mechanisms and molecular pathway changes of Tumor Treating Fields (TTFields) alone or in combination with radiotherapy and chemotherapy

Anti-cancer mechanisms of action of therapeutic alternating electric fields (tumor treating fields [TTFields])

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