## 1 Introduction  
Every year, approximately 527,600 women are newly diagnosed with cervical cancer, and 265,700 people die of cervical cancer [1]. Many efforts have been made to find or develop efficient anticancer drugs to treat cervical cancer and promote the survival rate [2]. The anticancer effect and mechanism of drugs were usually investigated through their performance in inducing cancer cell apoptosis [3; 4; 5]. Therefore, cervical cancer cells, i.e., HeLa cells, were widely used in drug-induced apoptosis studies to evaluate the anticancer effects and to investigate the anticancer mechanism of a drug or compound [6; 7; 8]. Recently, extracting active anticancer compounds from natural substances has attracted much attention due to their simple composition, strong stability, high safety, and low irritation [9; 10]. Cordycepin (3' deoxyadenosine), extracted from the Chinese traditional medicinal mushroom, _Cordyceps militaris_, is an adenosine analogue [11]. Cordycepin has been shown to interfere with biochemical and molecular processes such as purine biosynthesis [11; 12; 13], DNA/RNA synthesis [14], and mTOR (mammalian target of rapamycin) signaling transduction [15]. To date, the anticancer function of cordycepin was reported in several types of cancers, including human colorectal cancer [16],breast cancer [17], human leukemia [18], thyroid carcinoma [19], glioma [20], and human ovarian cancer [21]. Based on previous reports, cordycepin possibly induces apoptosis through regulating the expression of various proteins, inhabiting mRNA polyadenylation and/or reducing mitochondrial membrane potential [16; 17; 18; 19; 20; 21]. However, the mechanism of cordycepin-induced cancer cell apoptosis is still not completely clear and remains to be elucidated before using it clinically. Apoptosis, or programmed cell death, is an active gene regulation process that plays a crucial role in the growth and development of organisms and the removal of damaged cells [22]. Many anticancer drugs play a therapeutic role by inducing tumor cell apoptosis [23; 24]. In general, cells undergo specific characteristic changes during apoptosis. In the early stage, the cellular membrane shrinks, and the organelles are more tightly packed; in the late stage, the bond of DNA breaks, chromatin condensation and apoptotic bodies appear [25]. In correspondence, the contents of proteins and lipids as well as the concentration of nucleic acids and RNA may also change during cell apoptosis. Accurate measurement of these contents will provide insights in revealing the mechanisms in cell apoptosis. Cell apoptosis is often investigated using flow cytometry [26], fluorescence microscopy [27], electron microscopy [28], DNA electrophoresis [29], MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolzolium bromide) [30], and TUNEL (terminal deoxynucleotide) transferase dUTP nick end labeling) [31], etc. These approaches are effective, yet they usually include invasive procedures (e.g., cellular fluorescent labeling or cell fixation), which greatly limit the applications in live cells and longitudinal measurements [32]. Furthermore, many approaches only display structural appearance or identify the degradation of a single product and are not able to provide detailed changes in various contents in the cells at the same time. Raman spectroscopy, on the other hand, is a rapid, non-invasive technique that provides fingerprint information about the molecular structures of various contents by measuring the vibrational mode of molecules at once [33]. Raman spectroscopy has the characteristics of high-accuracy, high-sensitivity, non-invasiveness and real-time operation. It maintains the integrity and function of cells and simplifies the experimental procedure [34; 35]. Conventional Raman spectroscopy suffers from weak signals, especially in the complex biological environment. Yet, the emergence of surface-enhanced Raman spectroscopy (SERS) has provided a solution to this problem [36].