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# Sensitisation to Conventional Therapies

## Sensitisation to Conventional Therapies

### Overview

Across multiple cell-line and animal studies, apigenin increases the effect of standard anticancer therapies. In several models, the combined effect is greater than the drug alone.

That makes chemosensitisation one of the most clinically plausible short-term applications for apigenin in an active-treatment context. It remains promising rather than proven.

### How sensitisation works

Apigenin appears to sensitise cancer cells through several complementary mechanisms:

* lowering the apoptotic threshold by suppressing `BCL-2`, `BCL-xL`, and `MCL-1`
* stabilising and retaining p53 in the nucleus, amplifying DNA-damage responses
* reversing drug resistance, especially in `MCL-1`-high cisplatin-resistant cells
* suppressing SASP during and after treatment, reducing pro-survival signals from senescent stromal cells
* modulating autophagy, which in some resistant models shifts from a survival program toward cell death

### Evidence by drug

| Drug                      | Cancer Model                                                                        | Evidence Level                      |
| ------------------------- | ----------------------------------------------------------------------------------- | ----------------------------------- |
| Cisplatin                 | Lung, ovarian, colon, osteosarcoma — resistance reversal and synergistic apoptosis  | In vitro, with some in vivo support |
| Doxorubicin               | Hepatocellular carcinoma — recovery of drug efficacy in cell lines and mouse model  | In vitro + animal                   |
| Sorafenib                 | Hepatocellular carcinoma — enhanced antitumour efficacy in mouse model              | In vitro + animal                   |
| Paclitaxel                | Multiple solid tumours — reduced ROS-linked resistance                              | In vitro                            |
| 5-Fluorouracil            | Colorectal — stronger apoptosis and lower resistance                                | In vitro                            |
| Topoisomerase inhibitors  | Leukaemia — BCL-2 suppression and stronger apoptotic response                       | In vitro                            |
| Etoposide                 | Neuroblastoma — nuclear p53 retention and stronger DNA-damage response              | In vitro                            |
| Gemcitabine               | Pancreatic — sensitisation in cancer cell models                                    | In vitro                            |
| Olaparib (PARP inhibitor) | Solid tumours — restoration of drug sensitivity through survival-pathway modulation | In vitro                            |

Liposomal and other nano-formulations improve bioavailability and antitumour activity in preclinical models, but no human phase II oncology trials have defined clinical performance.

### What remains unknown

* safe and effective human doses for any chemosensitisation strategy
* best timing relative to chemotherapy administration
* whether CYP and transporter interactions alter safety or exposure with specific drugs
* long-term outcomes in any combination regimen

All sensitisation data remain preclinical.

### References

* Arango D, et al. [Apigenin enhances the cisplatin cytotoxic effect through p53-dependent apoptosis](https://pmc.ncbi.nlm.nih.gov/articles/PMC5351382/)
* Ding X, et al. [Apigenin induces apoptosis and counteracts cisplatin-induced resistance in ovarian cancer](https://pmc.ncbi.nlm.nih.gov/articles/PMC7388300/)
* Huang S, et al. [Apigenin enhances sorafenib anti-tumour efficacy in HCC](https://pubmed.ncbi.nlm.nih.gov/38394865/)
* Mahbub AA, et al. [The effect of apigenin and chemotherapy combination treatments on leukemia cells](https://pmc.ncbi.nlm.nih.gov/articles/PMC9132959/)
* Prasad S, et al. [Chemoprotective and chemosensitizing effects of apigenin on cancer therapy](https://pmc.ncbi.nlm.nih.gov/articles/PMC8555304/)


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